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Breeding

Pedigree Analysis and How Breeding Decisions Affect Genes

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Reprinted by permission, Jerold S Bell DVM

Jerold s Bell DVM, Clinical Associate Professor of Genetics, Tufts Cummings School of Veterinary Medicine

To some breeders, determining which traits will appear in the offspring of a mating is like rolling the dice – a combination of luck and chance. For others, producing certain traits involves more skill than luck – the result of careful study and planning. As breeders, you must understand how matings manipulate genes within your breeding stock to produce the kinds of offspring you desire.

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Photo by Dustin Hartje

When evaluating your breeding program, remember that most traits you’re seeking cannot be changed, fixed or created in a single generation. The more information you can obtain on how certain traits have been transmitted by your animal’s ancestors, the better you can prioritize your breeding goals. Tens of thousands of genes interact to produce a single individual. All individuals inherit pairs of chromosomes; one from the mother and one from the father. On the chromosomes are genes; so all genes come in pairs. If both genes in a pair are the same gene (for instance, “aa” or “AA”) the gene pair is called homozygous. If the two genes in a gene pair are unlike (for instance, “Aa”) the gene pair is called heterozygous. Fortunately, the gene pairs that make a cat a cat and not a dog are always homozygous. Similarly, the gene pairs that make a certain breed always breed true are also homozygous. Therefore, a large proportion of homozygous non-variable pairs – those that give a breed its specific standard – exist within each breed. It is the variable gene pairs, like those that control color, size and angulation that produce variations within a breed.

There are ways to measure the genetic diversity of a population. One method is to measure the average inbreeding coefficient (or Wright’s coefficient) for a breed. The inbreeding coefficient is a measurement of the genetic relatedness of the sire and dam. If an ancestor appears on both the sire and dam’s side of the pedigree, it increases the inbreeding coefficient. The inbreeding coefficient gives a measurement of the total percentage of variable gene pairs that are expected to be homozygous due to inheritance from ancestors common to the sire and dam. It also gives the chance that any single gene pair can be homozygous due to inheritance from ancestors common to the sire and dam. It also gives the chance that any single gene pair can be homozygous.

The types of matings that you choose for your breeding animals will manipulate their genes in the offspring, affecting their expression. Linebreeding is breeding individuals more closely related (a higher inbreeding coefficient) than the average of the breed. Outbreeding involves breeding individuals less related than the average of the breed. Linebreeding tends to increase homozygosity. Outbreeding tends to increase heterozygosity. Linebreeding and inbreeding can expose deleterious recessive genes through pairing-up, while outbreeding can hide these recessives, while propagating them in the carrier state.

Most outbreeding tends to produce more variation within a litter. An exception would be if the parents are so dissimilar that they create a uniformity of heterozygosity. This is what usually occurs in a mismating between two breeds, or a hybrid, like a Cockapoo. The resultant litter tends to be uniform, but demonstrates “half-way points” between dissimilar traits of the parents. Such litters may be phenotypically uniform, but will rarely breed true due to a mix of dissimilar genes.

One reason to outbreed would be to bring in new traits that your breeding stock does not possess. While the parents may be genetically dissimilar, you should choose a mate that corrects your breeding animal’s faults but complements its good traits. It is not unusual to produce an excellent quality individual from an outbred litter. The abundance of genetic variability can place all the right pieces in one individual. Many top-winning show animals are outbred. Consequently, however, they may have low inbreeding coefficients and may lack the ability to uniformly pass on their good traits to their offspring. After outbreeding, breeders may want to breed back to individuals related to their original stock, to attempt to solidify newly acquired traits.

Linebreeding attempts to concentrate the genes of specific ancestors through their appearance multiple times in a pedigree. It is better for linebred ancestors to appear on both the sire’s and dam’s sides of the pedigree. That way their genes have a better chance of pairing back up in the resultant offspring. Genes from common ancestors have a greater chance of expression with paired with each other than when paired with genes from other individuals, which may mask or alter their effects.

Linebreeding on an individual may not reproduce a outbred ancestor. If an ancestor is outbred and generally  heterozygous (Aa), increasing homozygosity will produce more AA and aa. The way to reproduce ab outbred ancestor is to mate two individuals that mimic the appearance and pedigree of the ancestor’s parents.

Inbreeding significantly increases homozygosity, and increases the expression of both desirable and deleterious recessive genes through pairing up. If a recessive gene (a) is rare in the population, it will almost always be masked by a dominant gene (A). Through inbreeding, a rare recessive gene (a) can be passed from a heterozygous  (Aa) common ancestor through both the sire and dam, creating a homozygous recessive (aa) offspring.

The total inbreeding coefficient is the sum of the inbreeding from the close relatives (first cousin mating), and the background inbreeding from common ancestors deep in the pedigree. Such founding ancestors established the pedigree base for the breed.
The total inbreeding coefficient is the sum of the inbreeding
from the close relatives (first cousin mating), and the
background inbreeding from common ancestors deep in the
pedigree. Such founding ancestors established the pedigree
base for the breed.

Knowledge of the degree of inbreeding in a pedigree does not necessarily help you unless you know whose genes are being concentrated. The relationship coefficient, which can also be approximated by what is called the percent blood coefficient, represents the probable genetic likeness between the individual whose pedigree is being studied, and a particular ancestor.

We know that a parent passes on an average of 50% of its genes, while a grandparent passes on 25%, a great-grandparent 12.5%, and so on. For every time the ancestor appears in the pedigree, its percentage of passed on genes can be added up and its “percentage of blood” estimated. In many breeds, an influential individual may not appear until later generations, but then will appear so many times that it necessarily contributes a large proportion of genes to the pedigree.

The average inbreeding coefficient of a breed is a measurement of its genetic diversity. When computing inbreeding coefficients, you have to look at a deep pedigree to get accurate numbers. An inbreeding coefficient based on 10 generation pedigrees is standardly used, but requires a computerized pedigree database to compute.

The average inbreeding coefficient for a breed will be based on the age and genetic background of the breed. A mating with an inbreeding coefficient of 14 percent based on a ten generation pedigree, would be considered moderate inbreeding for a Labrador Retriever (a popular breed with a low average inbreeding coefficient), but would be considered outbred for an Irish Water Spaniel (a rare breed with a higher average inbreeding coefficient).

Most breeds start from a small founding population, and consequently have a high average inbreeding coefficient. If a breed is healthy and prolific, the breadth of the gene pool increases, and the average inbreeding coefficient can go down over time. Some dog breeds were established on a working phenotype, and not on appearance. These breeds usually start with low inbreeding coefficients due to the dissimilar backgrounds of the founders. As certain individuals are linebred on to create a uniform physical phenotype, the average inbreeding coefficient can increase.

There is no specific level or percentage of inbreeding that causes impaired health or vigor. If there is no diversity (non-variable gene pairs for a breed) but the homozygote is not detrimental, there is no effect on breed health. The characteristics that make a breed reproduce true to its standard are base on non-variable gene pairs. There are pure-bred populations where smaller litter sizes, shorter life expectancies, increased immune-mediated disease, and breed-related genetic disease are plaguing the population. In these instances, prolific ancestors have passed on detrimental recessive genes that have increased in frequency and homozygosity. With this type of documented inbreeding depression, it is possible that an outbreeding scheme could stabilize the population. However, it is also probable that the breed will not thrive without an influx of new genes; either from a distantly related (imported) population, or crossbreeding.

Fortunately, most breeds do not find themselves in the position of this amount of limited diversity and inbreeding depression. However, the perceived problem of a limited gene pool has caused some breeders to advocate outbreeding of all individuals. Studies in genetic conservation and rear breeds have shown that his practice contributes to the loss of genetic diversity. By uniformly crossing all “lines” in a breed, you eliminate the differences between them, and therefore the diversity between individuals. Eventually, there will not be any “unrelated line” to be found. Everyone will have a mixture of everyone else’s genes. The practice in livestock breeding has significantly reduced diversity, and caused the reduced diversity, loss of unique rare breeds.

A basic tenet of population genetics is that gene frequencies do not change from generation to generation. This will occur regardless of the homozygosity or heterozygosity of the parents, or whether the mating is an outbreeding, linebreeding, or inbreeding. This is the nature of genetic recombination. Selection, and not the types of matings used affect gene frequencies and breed genetic diversity.

If two parents are both heterozygous (both Aa) for a gene pair, on the average, they would produce 25% AA, 50% Aa, and 25% aa. (These are the averages when many litters are combined. In reality, any variety of pairing up can occur in a single litter.) If a prolific male comes out of this litter, and he is homozygous aa, then the frequency of the “a” gene will increase in the population, and the frequency of the “A” gene will decrease. This is known as the popular sire syndrome. Of course, each individual has thousands of genes that vary in the breed, and everyone carries some deleterious recessive genes. The overuse of individual breeding animals contributes the most to decreased diversity (population bottlenecks), and the increased spread of deleterious recessive genes (the founders effect). Again, it is selection (use of this stud to the exception of others), and not the types of matings he is involved in that alters gene frequencies. Breeders should select the best individuals from all lines, so as to not create new genetic bottlenecks.

Decisions to linebreed, inbreed or outbreed should be made based on the knowledge of an individuals traits and those of its ancestors. Inbreeding will quickly identify the good and bad recessive genes the parents share, based on their expression in the offspring. Unless you have prior knowledge of what the offspring of milder linebreedings on the common ancestors were like, you may be exposing your litters (and buyers) to extraordinary risk of genetic defects. In your matings, the inbreeding coefficient should only increase because you are specifically linebreeding (increasing the percentage of blood) to selected ancestors.

Don’t set too many goals in each generation, or your selective pressure for each goal will necessarily become weaker. Genetically complex or dominant traits should be addressed early in a long-range breeding plan, as they may take several generations to fix. Traits with major dominant genes become fixed more slowly, as the heterozygous (Aa) individuals in a breed will not be readily differentiated from the homozygous-dominate (AA) individuals. Desirable recessive traits can be fixed in one generation because individuals that show such characteristics are homozygous for the recessive genes. Individuals that pass on desirable traits for numerous matings and generations should be preferentially selected for breeding stock. This prepotency is due to homozygosity of dominate (AA) and recessive (aa) genes. However, these individuals should not be overused, to avoid the popular sire syndrome.

Breeders should plan their matings based on selecting toward a breed standard, based on the ideal temperament, performance, and conformation, and should select against the significant breed related health issues. Using progeny and sib-based information to select for desirable traits and against detrimental traits will allow greater control.

This article can be reproduced with the permission of the author. Jerold.Bell@tufts.edu

 

Breeding

Furnishings and the Three Genes That Account for Them

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Thank you Silvia Timmermann for the various photographs used here to show the differences in the Gordon Setter furnishings.

From: National Purebred Dog Day

NPPD published this interesting article that explains how the furnishings on our Gordon Setter are inherited.

Furnishings, and Three Genes That Account for Them

December 21, 2016 | 2 Comments

“Furnishings” doesn’t refer just to furniture. The word itself is quite old and can be traced to back the 16th century and the Middle French word, “fournir,” which morphed into “fourniture”  to mean “a supply,” or the act of furnishing. In the dog world, “furnishings” refers to long hair on the extremities of certain breeds. In some wire-haired breeds, it can refer to a longer mustache, beard and eyebrows, while in setters, furnishings refers to the flowing hair coming off the dog’s body.

coat0Interestingly, variants in only three genes govern coat length, curl and furnishings. It was something discovered in 2009 by Edouard Cadieu and Elaine A. Ostrander of the National Human Genome Research Institute who looked at some 900 dogs representing 80 breeds. They were able to identify mutations at specific points, or loci, on three genes linked to fur length, curliness and growth pattern (what we call “furnishings”).  When they looked at the three loci on the genes of another 662 dogs representing 108 breeds — from Old English Sheepdogs to Pugs – they found that the presence of the mutations or not, in various combinations, accounted for the variation in coat in 95 percent of the breeds. Only a few breeds, including Afghan hounds, have coats that can’t be explained by these genes.

Here is the link to the study itself:

Coat Variation in the Domestic Dog Is Governed by Variants in Three Genes

Edouard Cadieu,1 Mark W. Neff,2 Pascale Quignon,1 Kari Walsh,2 Kevin Chase,3 Heidi G. Parker,1 Bridgett M. VonHoldt,4 Alison Rhue,2 Adam Boyko,5 Alexandra Byers,1 Aaron Wong,2 Dana S. Mosher,1 Abdel G. Elkahloun,1Tyrone C. Spady,1 Catherine André,6 K. Gordon Lark,3 Michelle Cargill,7,* Carlos D. Bustamante,5 Robert K. Wayne,4and Elaine A. Ostrander1,†

Abstract

coat11Coat color and type are essential characteristics of domestic dog breeds. Although the genetic basis of coat color has been well characterized, relatively little is known about the genes influencing coat growth pattern, length, and curl. We performed genome-wide association studies of more than 1000 dogs from 80 domestic breeds to identify genes associated with canine fur phenotypes. Taking advantage of both inter- and intrabreed variability, we identified distinct mutations in three genes, RSPO2, FGF5, and KRT71 (encoding R-spondin–2, fibroblast growth factor–5, and keratin-71, respectively), that together account for most coat phenotypes in purebred dogs in the United States. Thus, an array of varied and seemingly complex phenotypes can be reduced to the combinatorial effects of only a few genes.

The tremendous phenotypic diversity of modern dog breeds represents the end point of a >15,000-year experiment in artificial and natural selection (1, 2). As has been demonstrated for traits such as body size (3) and coat color (4), marker-based associations with phenotypic traits can be explored within single breeds to initially identify regions of genetic association, and then expanded to multiple breeds for fine-mapping and mutation scanning (5, 6). Coat (pelage) phenotypes are particularly amenable to this strategy as they show a huge amount of variation across breeds but still allow for simple variation within single breeds (7). This offers a unique strategy for advancing the genetic understanding of a complex phenotype.

coat8We used the structured pattern of fur variation in dogs to localize the genetic basis of three characteristics of the canine coat: (i) the presence or absence of “furnishings,” the growth pattern marked by a moustache and eyebrows typically observed in wire-haired dogs; (ii) hair length; and (iii) the presence or absence of curl. To accomplish this, we generated three genome-wide single-nucleotide polymorphism (SNP) data sets using the Affymetrix version 2.0 canine SNP chip (8, 9). The first data set consisted of 96 dachshunds segregating three coat varieties: wire-haired with furnishings, smooth, and long-haired without furnishings. The second data set comprised 76 Portuguese water dogs (PWDs), segregating the curl phenotype. The final data set, termed CanMap, included 903 dogs from 80 breeds representing a wide variety of phenotypes. An additional data set used to map furnishings included a panel of microsatellite markers (10), genotyped on a 96-dachshund pedigree segregating all three coat varieties.

coat5The same strategy was used to map all three traits. First, a genome-wide association study (GWAS) within a breed segregating the phenotype was conducted to determine the most strongly associated locus. To rule out false-positives caused by population structure within the breeds (11), we did a second GWAS that used the CanMap data set divided into cases and controls based on the presence or absence of the phenotype in question. Fine-mapping of significant, concordant peaks was used to define the smallest shared haplotype, followed by sequencing to identify the putative causative mutations. Each mutation was validated in a large panel of at least 661 dogs from 108 breeds, including cases and controls for all phenotypes (table S1).

We initially mapped furnishings in the dachshund using smooth-coated and long-haired dogs as controls and wire-haired dogs as cases (Fig. 1A). Single-marker analysis of the dachshund GWAS data set and concurrent linkage analysis of the dachshund pedigree identified the same locus on canine chromosome 13 (CFA13) surrounding nucleotide 11,095,120 [P = 3.4 × 10−27, lod score (logarithm of the odds ratio for linkage) = 5.6; Fig. 1B]. We confirmed the association on CFA13 in the CanMap data set at nucleotide 11,659,792 (P = 10−241; Fig. 1C and table S2). A 718-kb homozygous haplotype in all dogs fixed with furnishings was located within both the original 3.4-Mb haplotype observed in the dachshund-only GWAS, and a 2.8-Mb haplotype identified in crossover analysis within the dachshund pedigree (Fig. 1D).

Fig. 1

GWAS and fine-mapping identify RSPO2 as the associated gene for moustache and eyebrow growth pattern (furnishings). (A) Three types of coat segregate in dachshunds: (from left to right) smooth-coated, long-haired, and wire-haired with furnishings. (B …

Fine-mapping allowed us to reduce the homozygous region to 238 kb spanning only the R-spondin–2 (RSPO2) gene, excluding the 5′ untranslated region (5′UTR) and the first exon (Fig. 1D, fig. S1, and table S3). RSPO2 is an excellent candidate for a hair-growth phenotype as it synergizes with Wnt to activate β-catenin (12), and Wnt signaling is required for the establishment of the hair follicles (13, 14). Moreover, the Wnt/β-catenin pathway is involved in the development of hair-follicle tumors, or pilo-matricomas (15), which occur most frequently in breeds that have furnishings (16). Recent studies have shown that a mutation in the EDAR gene, also involved in the Wnt pathway, is responsible for a coarse East-Asian hair type found in humans (17), with some similarity to canine wirehair.

All exons and conserved regions of RSPO2 were sequenced in dogs from seven breeds (table S4). Only an insertion of 167 base pairs (bp) within the 3′UTR at position 11,634,766 was perfectly associated with the furnishings trait in dogs from both the case/control study and the extended pedigree (table S5). The result was further confirmed in a set of 704 dogs of varying phenotypes. In total, 297 of 298 dogs with furnishings were either homozygous (268) or heterozygous (29) for the insertion, and all 406 dogs lacking the trait were homozygous for the ancestral state, as is consistent with a dominant mode of inheritance (table S1).

This mutation does not affect the protein-coding region of the RSPO2 gene. However, because the 3′UTR frequently encodes elements that influence mRNA stability [reviewed in (18)], we examined whether the insertion was associated with a change in the expression level of the RSPO2 gene. We found a threefold increase in RSPO2 transcripts in muzzle skin biopsies of dogs with furnishings, consistent with a transcript effect (fig. S2).

We applied the same mapping strategy to hair length. Previously, mutations in the FGF5 gene were identified in Welsh corgis segregating an atypical “fluffy” or long-haired phenotype (19) and associated with excess hair growth in mice and cats (20–22). Our study replicates these findings in an extended breed set. Indeed, association analyses in both the dachshund and CanMap data sets highlight the region on CFA32 containing FGF5 with P values of 3 × 10−27 and 9 × 10−44, respectively. After fine-mapping, a 67-kb homozygous region highlighted the FGF5 gene (Fig. 2A, fig. S3, and table S6). The strongest association was observed at position 7,473,337 (P = 1 × 10−157), in which a highly conserved Cys is changed to Phe (Cys95→Phe) in exon 1 of FGF5, consistent with the previous study (19). Sequencing within the homozygous haplotype revealed no SNPs with stronger association (table S7).

Fig. 2

Regions of homozygosity identify genes for pelage length and curl. (A) Homozygous region found on CFA32 defining the length locus. The red bar indicates the 520-kb associated haplotype from 29 long-haired dachshunds; the blue bar spans the 125-kb homozygous …

This diagnostic SNP was typed in several hundred additional dogs of varying hair length. Within the dachshunds, all long-haired dogs had the TT genotype, whereas all short or wire-haired dogs had either the GT or GG genotypes, suggesting a recessive mode of inheritance, as predicted previously (23). Across all breeds, the T allele was found in 91% of the long-haired dogs, in only 3.9% of the short-haired dogs, and accounts for ~30% of genotypes found in medium-haired dogs. Three breeds with very long hair, including the Afghan hound, neither carry the Cys95→Phe variant nor show an association with CFA32, suggesting that additional loci exist that contribute to hair length in dogs (table S1).

To identify the gene that causes curly coat, we conducted a GWAS using PWDs (Fig. 2B) and identified a single associated SNP at position 5,444,030 on CFA27 (P = 4.5 × 10−7). A SNP in close proximity (5,466,995; P = 6.9 × 10−28) was associated with curly coat in the CanMap data set. Fine-mapping revealed a shared homozygous haplotype that included two keratin genes (Fig. 2C, fig. S4, and table S8). Sequence data covering 87% of the homozygous region identified one SNP at position 5,542,806 that segregated with the trait. Non–curly haired dogs carried the CC genotype; curly coated dogs had the TT genotype. In breeds where the trait segregates, such as PWDs, all three genotypes were observed. The relevant SNP is located in the KRT71 gene (previously called K6irs1, Kb34, and K71) and causes a nonsynonymous Arg151→Trp alteration (table S9). Genotyping an additional 661 samples at this SNP validated the association (P = 3 × 10−92) (table S1).

Keratins are obvious candidates for hair growth [reviewed in (24)], and mutations in KRT71 have been described in curly coated mice (25). The mutation described in our study is within the second exon of the gene and may affect either or both of two protein domains: a coiled-coil and a prefoldin domain (www.ensembl.org/Canis_familiaris/). Conceivably, sequence alterations in these domains could affect cellular targeting, receptor binding, or proper folding of the protein after translation [reviewed in (26)].

Notably, these three mutations in various combinations explain the observed pelage phenotype of 95% of dogs sampled, which include 108 of the ~160 American Kennel Club (AKC)–recognized breeds. A total of 622 dogs representing all identifiable coat phenotypes were genotyped at all three loci (table S10). By analyzing each of the three major traits both within and across multiple breeds, we show that combinations of these genotypes give rise to at least seven different coat types, encompassing most coat variation in modern domestic dogs (Fig. 3). Specifically, short-haired breeds display the ancestral state in all three genes. Wire-haired breeds, all of which have furnishings, carry the RSPO2 insertion. Dogs that carry both the RSPO2 and KRT71 mutations display “curly-wire” hair that is similar in texture to wire-hair but longer and curled or kinked rather than straight. Long-haired breeds carry the variant form of FGF5. Dogs carrying the FGF5 mutation, along with the RSPO2 insertion, have furnishings and long soft coats, rather than wiry ones. When dogs carry variants in both FGF5 and KRT71, the pelage is long and curly. Not surprisingly, coats must be of sufficient length to curl, and all curly haired dogs in our study were homozygous for the FGF5 mutation. Finally, if all three mutations are present, the phenotype is long and curly with furnishings.

Fig. 3

Combinations of alleles at three genes create seven different coat phenotypes. Plus (+) and minus signs (−) indicate the presence or absence of variant (nonancestral) genotype. A characteristic breed is represented for each of the seven combinations …

None of the mutations we observed were found in three gray wolves or the short-haired dogs, indicating that short-haired dogs carry the ancestral alleles (table S1). Our finding of identical haplotypes surrounding the variants in all dogs displaying the same coat type suggests that a single mutation occurred for each trait and was transferred multiple times to different breeds through hybridization. Because most breeds likely originated within the past 200 years (27), our results demonstrate how a remarkable diversity of phenotypes can quickly be generated from simple genetic underpinnings. Consequently, in domesticated species, the appearance of phenotypic complexity can be created through combinations of genes of major effect, providing a pathway for rapid evolution that is unparalleled in natural systems. We propose that in the wake of artificial selection, other complex phenotypes in the domestic dog will have similar tractable architectures that will provide a window through which we can view the evolution of mammalian form and function.

Supplementary Material

Supplementary Data

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Acknowledgments

We gratefully acknowledge support from NSF grants 0733033 (R.K.W.) and 516310 (C.D.B.), NIH grants 1RO1GM83606 (C.D.B.) and GM063056 (K.G.L. and K.C.), the Nestlé Purina company, the AKC Canine Health Foundation, the University of California–Davis Veterinary Genetics Laboratory, and the Intramural Program of the National Human Genome Research Institute. We thank L. Warren and S. Stafford for providing pictures. Finally, we thank the many dog owners who generously provided us with samples from their pets.

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Footnotes

Supporting Online Material

www.sciencemag.org/cgi/content/full/1177808/DC1

Materials

Materials and Methods

Figs. S1 to S5

Tables S1 to S10

References

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References and Notes

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4. Karlsson EK, et al. Nat Genet. 2007;39:1321. [PubMed]
5. Lindblad-Toh K, et al. Nature. 2005;438:803. [PubMed]
6. Wayne RK, Ostrander EA. Trends Genet. 2007;23:557. [PubMed]
7. American Kennel Club. The Complete Dog Book. 19. Howell Book House; New York, NY: 1998.
8. Drogemuller C, et al. Science. 2008;321:1462. [PubMed]
9. Materials and methods can be found at Science Online.
10. Wong AK, Neff MW. Anim Genet. 2009;40:569. [PubMed]
11. Lander ES, Schork NJ. Science. 1994;265:2037. [PubMed]
12. Kazanskaya O, et al. Dev Cell. 2004;7:525. [PubMed]
13. Andl T, Reddy ST, Gaddapara T, Millar SE. Dev Cell. 2002;2:643. [PubMed]
14. Clevers H. Cell. 2006;127:469. [PubMed]
15. Chan EF, Gat U, McNiff JM, Fuchs E. Nat Genet. 1999;21:410. [PubMed]
16. Meuten DJ, editor. Tumors in Domestic Animals. 4. Blackwell; Ames, Iowa: 2002.
17. Mou C, et al. Hum Mutat. 2008;29:1405. [PubMed]
18. Chatterjee S, Pal JK. Biol Cell. 2009;101:251. [PubMed]
19. Housley DJ, Venta PJ. Anim Genet. 2006;37:309. [PubMed]
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Breeding, Health & Genetics

Let’s Talk Linebreeding

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“One of the most bandied about terms among … breeders today seems to be linebreeding. Despite it’s widespread use, however, linebreeding is frequently misunderstood and miscommunicated; in fact, it is not altogether uncommon for an outcrossed pedigree to be mistakenly viewed as linebreeding by the novice. The present discussion defines linebreeding and how we can more accurately define our linebred litters.”

From – “Let’s Talk Linebreeding” written by Claudia Waller Orlandi, Ph.D. published in ‘Tally Ho’ the Basset Club of America Newsletter (July-August ’97). The online article may be found by clicking here.

(While this article was written with the Basset Hound breeder in mind, one can change the name to  Gordon Setter, or any breed for that matter, as the material is “one size fits all” when it comes to the topic of breeding.)

Linebreeding and Inbreeding: A Family Affair

Inbreeding and Linebreeding involve the mating of animals within the same family. Breeding relatives is used to cement traits, the goal being to make the offspring homozygous (pure) for desirable characteristics. Homozygous dogs tend to be prepotent and produce offspring that look like themselves (Walkowicz & Wilcox 1994)

Willis (1989) defines Inbreeding as the mating of animals “more closely related to one another than the average relationship within the breed.” Inbred pairings would include brother/sister (the closest form) father/daughter, mother/son, and half-brother/half-sister.  Linebreeding involves breeding relatives other than the individual parents or brother and sisters. Typical linebred matings are grandfather/granddaughter, grandmother/grandson, grandson/granddaughter, great-grandmother/great-grandson, uncle/niece, aunt/nephew and cousin crosses. Linebreeding is a less intense form of inbreeding. Because of their focus on a dog’s potential genetic contribution, inbreeding and line breeding are termed genetic breeding systems.

figure-1-genetic-breeding-systems Definition:  For a dog to be linebred there must be an ancestor in the pedigree that is common to both the sire and the dam.  Figure 2 illustrates this concept. Kelly is linebred because the dog, Brahms, appears twice in the sire’s side and once in the dam’s side of the pedigree.figure-2-linebreedingCommon Misconception:  A pedigree may show either the sire and/or the dam to be linebred but no ancestor common to both the sire and dam. This is outcrossing, not linebreeding (see figure 3).  Similarly, because the same kennel prefixes (Windy, Hill, Castle) are common to both the sire’s and dam’s ancestors, the newcomer may mistakenly view the pedigree as linebreeding.figure-3-outcrossingWhere to draw the “Line”?

Breeders do not always agree on what constitutes linebreeding, with some feeling that common ancestors within the first five or six generations is linebreeding. Willis (1989) indicates that the farther back linebreeding is in a pedigree the less intensive it will be, pointing out that a dog appearing 12 times (out of a possible 32) in the 6th generation of a pedigree would have a Coefficient of Inbreeding (CI) of only 1.8% (by comparison, a sire to a granddaughter cross has a CI of 12.5%). The CI tell us the proportion of genes for which the inbred ancestor is likely to be homozygous, that is carrying the same genes from each parent. (Remember that homozygous animals have a higher potential for reproducing themselves.) In Willis’s (1992) view, a common ancestor farther back than the 2nd or 3rd generation will have little influence on the litter. Linebreeding beyond the fourth generation has even less genetic impact.

How much bang will we get for our buck (or Basset!)

Several modern writers (Walkowitz & Wilcox 1994; Willis 1992, 1989; Onstott 1962) view linebreeding and inbreeding as essentially the same  and differing only in degree of intensity. Whether one considers inbreeding and linebreeding to be the same or feels they are two distinct breeding systems, quantifying the degree to which an animal is linebred (or inbred) provides important information regarding its potential genetic contribution. As Willis (1989) states: “When describing inbreeding [or linebreeding] breeders often say their dog is inbred or linebred without further qualification. This is a very inadequate description. We need to know which dog the animal is inbred [linebred] to and the degree of inbreeding [linebreeding].” Put another way, how much “bang” will we get from our linebreeding?

Describing your Basset’s linebred pedigree: reading, writing and a little arithmetic!

Willis (1992) suggests that a concise yet meaningful way to express the extent of linebreeding (inbreeding) is to number the generations of the animal in question. The common ancestor(s) is assigned the generation number as he/she appears in the pedigree. The parents are the first generation (1), the grandparents are the second (2), great grandparents are the third (3), great-great-grandparents are the fourth (4) and so on.

As previously stated, Kelly’s pedigree (Figure 2) is an example of  linebreeding, with Brahms appearing on both the sire’s and dam’s side. On the sire’s side Brahms appears twice in the third generation (3). We can write this as 3.3. On the dam’s side, Brahms appears once in the second generation (2) and this is written simply as 2. Willis has suggested the following written and verbal formats for expressing the extent of line breeding in a pedigree:

Written Format

We would write: “Kelly is linebred on Brahms 3.3/2”

Verbal Format

We would say: “Kelly is linebred on  Brahms three, three TO two.”

In the Written Format notice we separate the sire’s and dam’s side of the pedigree by using a slash mark (think of a pencil making a slash mark); in the Verbal Format the word “TO” is used to separate the sire’s and dam’s side (think of talking “to” someone). This verbal and written format tells us the dog on which Kelly is linebred and the extent of the linebreeding. Smaller numbers indicate that a dog is more closely linebred; larger numbers of 4 and above (Willis 1989) indicate a lesser extent.

Linebreeding and pedigrees: a final caveat

Linebreeding and inbreeding are essentially the same, differing only in the degree of intensity. (In Willis’s view, the common ancestors beyond the 2nd and 3rd generations will not greatly influence the resulting litter.) We have described the ease with which an animal’s extent of linebreeding may be expressed by means of written and verbal models. Perhaps this format will be “adopted” by those Basset Hound breeders whose interest lies in linebreeding. In addition to facilitating the description of a linebred pedigree over the phone, it certainly provides important information regarding the potential outcome of a breeding. In this regard, two things bear repeating: (1) linebreeding (and inbreeding) are only as viable as a breeder’s knowledge of basic genetics (a topic which will be addressed in future columns) and (2) a linebred pedigree is only as valuable as a person’s ability to determine the virtues and faults of the dogs it contains. When we add the final ingredient of rigorous selection hopefully we are on the way to producing better Basset Hounds!

References

Onstott, K. 1980. The New Art of Breeding Better Dogs. Howell, New York.

Walkowicz, C. and Wilcox, B. 1994 Successful Dog Breeding. Howell, New York.

Will, M.B. 1968 A simple method for calculating Wright’s coefficient of inbreeding. Rev. Cubana Cienc.Agric. (Eng.Ed.) 2: 171-4

Willis, M.B. 1989 Genetics of the Dog. Howell, New York

Willis, M.B. 1992. Practical Genetics for Dog Breeders. Howell, New York

For more articles about breeding by Claudia follow the link below.

These articles were written by Claudia Waller Orlandi, Ph.D. All have been published in ‘Tally Ho’, the official newsletter of the Basset Hound Club of America

Thank you to Barbara Manson, WI for sharing this link with us.

Sally Gift, Mesa AZ

Photography by Susan Roy Nelson

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Breeding, Catch All

Communicating the Truth About Purebred Dogs

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For some time now I’ve stated that I believed that the activity of Animal Rights groups to promote the adoption of shelter dogs has been a leading cause in the decline of the purebred dog. This month the AKC has published a report and introduced action that we, as purebred lovers and breeders need to be aware of. If the purebred dog is to survive, if pet ownership is to survive, support for this AKC effort, from us as individuals and as well as our parent clubs will be needed.

Sally Gift, Mesa AZ

The following article appears in the Chanine Chronicle and can be access by clicking here.

September Chairman’s Report

 

New York, NY – Last Thursday we posted a charming photograph of three Golden Retriever puppies on the American Kennel Club Facebook page. The caption was “I love my breeder” with a request to “share your love for your dog’s breeder.”  The image was shared 2,500 times, received 11,000 likes and almost 500 comments. We posted this because we love responsible breeders, but also because we wanted to see the reaction it would elicit.

The post sparked a lengthy conversation about the merits of finding your new dog at a breeder vs. adopting a dog. That passionate debate proved two important issues. There are ardent, articulate, and knowledgeable supporters of responsible breeding who possess facts and are capable of persuasively educating the public about the truth of responsible breeding. However, it also proved that there is a great deal of misinformation about responsible breeding that result in significant prejudice against breeders. There is no doubt that prejudice against breeders has impacted our breeders, our sport, and the public’s ability to enjoy the unique experience of a purebred dog in their lives.

Just 20 years ago, a purebred dog was the dog to have in your life. Twenty years ago, a responsible breeder was viewed as a respected resource. Twenty years ago there were virtually no important legislative efforts aimed at eradicating all dog breeding.

What changed in those 20 years? The noble quest to give every dog a “forever” home was co-opted by the animal rights organizations as a method to raise funds for their mission to completely eliminate pet ownership. Under the guise of supporting adoption, they have been raising a significant war chest – over $200 million last year alone – to fuel a campaign aimed squarely at destroying our ability to preserve breeds for future generations.

As told by AR groups, responsible breeders have been dishonestly accused of being the sole cause of dogs in shelters – not irresponsible owners.

As told by AR groups, purebred dog breeders have been maliciously portrayed as evil people only interested in money and winning at events, at the expense of their dogs’ health and well-being.

As told by AR groups, purebred dogs have been wrongly defined as being plagued with genetic health and temperament problems caused by breeders.

After 20 years of this propaganda – mostly unchallenged by those who know better – a portion of the public has accepted this fiction as reality.

No more.

AKC Staff led by Chris Walker along with Bob Amen and I have been working with Edelman, our new public outreach partner, on the plan that will change the current conversation, as demonstrated in that Facebook post, by confronting the prejudice and telling the truth about purebred dogs and their responsible breeders.

We will focus our efforts on two key audiences – families with kids 8-12 and empty nesters. These groups represent the critical inflection points for dog ownership and hold our best opportunities to correctly educate the public about purebred dogs and responsible dog breeding.

An additional audience will be federal and local legislators. Our experience makes it clear that once legislators know the truth, the legislative outcome is positive.

We will expand our voice to include breeders, dog owners, AKC thought leaders, veterinarians, and AKC’s over 700,000 grassroots followers.

We will relentlessly focus on these foundational story themes: the unique qualities of purebred dogs, the desirability of purebred dogs as family pets, the truth about the health of purebred dogs, and the truth about responsible breeders.

We will use every outreach channel to relentlessly tell our story in a shareable and searchable way, including national and local media, hybrid media, AKC’s own media, and social media.

By focusing on these key audiences with expanded, credible voices centered on our core narratives we will get better stories in the media, more often.

In addition, we will immediately and aggressively respond to any attack utilizing our partners, our supporters, and our full media assets.

There are three things you can do to help regain control of our destiny.

Tell us what you are hearing from your community, what the toughest questions are that you face. We’ll compile the answers and get you a toolkit to respond from a position of knowledge, strength, and pride.

Tell us your story – how you picked your breed, why you became a breeder and what has changed about the health of your breed due to the efforts of your Parent Club.

Tell us who you know who can help tell the truth – supportive officials in parent, children’s, or seniors’ organizations either locally or nationally; a veterinarian who is actively involved in a professional organization either locally or nationally; or an informed and outspoken government official.

You can share all of this information with Chris Walker at cxw2@akc.org or 212-696-8232.

As an avid Bullmastiff breeder, I am reminded of the description of that great protector of the family and property – fearless and confident, yet docile. I believe the AKC is a great protector of our rights to responsibly breed dogs. We too are fearless and confident, but it is time to stop being docile regarding the lies and propaganda that defile purebred dogs and responsible breeders.

We will communicate the truth about purebred dogs and their responsible breeders, emotionally and memorably.

We will increase the desire to own a purebred dog.

We will de-stigmatize responsible breeders.

We will change the conversation.

We will change the future.

As always, your comments are most welcome at atk@akc.org.

Sincerely,

Alan Kalter

Chairman

Short URL: http://caninechronicle.com/?p=32967

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Catch All

The Dog Lover

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The Dog Lover takes a hard, inside look at the agenda of animal rights groups and will leave you questioning the tactics used to achieve their goals. Based on a true story, The Dog Lover tells the story of a young woman who goes undercover for an animal advocacy group to collect evidence against a breeder (played James Remar) the group believes is neglecting his dogs.

 

Breed Standard, Dog Shows

Impressions

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Another chapter in our review of the Gordon Setter breed standard

Barb Manson

Written by  Barbara Manson

There are a few things that we need to tie together in regard to the standard.  I’ve discussed most of the pieces but we need to see how they work together to create a good quality Gordon Setter.  As breeders and exhibitors, it’s important that we not “fool” ourselves as we evaluate our own dogs and those of our competitors.  We want what’s best for our breed and we need to be confident and articulate in regards to our choices.  We must also establish, in our own minds, what represents a correct Gordon Setter and what is simply personal preference.  These can be two separate things.  By so doing, we are keeping our minds open and we are better able to evaluate the qualities found in competitors dogs.  This is vital if we are to advance our breed.

Impressions
Photo by Ben Perez, 2016 GSCA National Specialty

 

What does the judge see when he/she is evaluating our dogs on the go around.  We all know he sees dogs who may be limping.  These dogs are usually excluded from competition because they are considered unsound on that day.  If you’re new, and this happens to you, don’t worry.  This has happened to most of us at one time or another.  Though disheartening, you will compete another day.  There are many other things that can be seen from the judge’s vantage point.  Under general appearance, size is mentioned.  I’ve covered this previously, but the judge can do an initial comparison between competitors at this point.  He should also see an “active, upstanding and stylish” dog ” appearing capable of doing a full day’s work in the field”.  Balance, and how all the pieces I’ve discussed fit together, is also apparent.  A “long, lean” neck, a “rather short back” and “a short tail” can be seen along with a correct topline on the move.  The expectation is a “high head carriage” and a back that remains relatively level on the move, not running down hill or overly slopingshoulder to rear.  The correctness of the tailset and its relationship to the croup is in evidence at this point.  The tail should appear as an extension of the back and be “carried horizontal or nearly so”.  The gait should be “bold, strong, driving and free-swinging”.  The tail flags constantly while the dog is in motion”.  So what constitutes a “free-swinging” gait?  It is a “smooth flowing, well balanced rhythm, in which the action is pleasing to the eye, effortless, economical and harmonious”.   The dog moves so easily it seems as though he is floating and could move that way all day without tiring.  If you’re the handler of such a dog, you can actually feel him ” collect” himself as he starts to move.

Impressions2
Photo by Ben Perez, 2016 GSCA National Specialty

Temperament also comes into play here.  He appears, at this point, “alert, gay, interested and confident”.  He is “fearless and willing”.  Many of us have had the experience of trying to show a dog who was not exactly “willing”.  It’s not what we want to see in the ring but when this happens, I prefer to think of them as “strong minded enough to stand the rigors of training”.  Some are just more strong minded than others.  We’ll discuss training techniques another day but this can be one of the challenges of showing a Gordon Setter.  It may take time and patience, but even the tough nuts can be cracked.  As you consider the importance of these impressions, remember, they are the first thing the judge sees on the initial go around.  He sees them again when your dog is evaluated individually, and they are the last thing he sees before he points his finger.  These impressions are big clues as to the dog’s ability to withstand a long day in the field.  Dogs who exhibit these attributes are a pleasure to watch and they draw your eye to them.  They may seem elegant but closer examination should reveal substance.  They are, after all, Setters.

Impressions5
Photo by Ben Perez, 2016 GSCA National Specialty

I’ve had a couple of people bring up the amount of coat we are seeing in the ring today.  Heavily coated dogs are certainly much more prevalent today than they were when I came into the breed.  You can look back through old reviews and see how this factor has changed.  The current standard only addresses coat as “soft and shining, straight or slightly waved, but not curly”.  It goes on to describe where the long coat appears, but gives no parameters regarding how much coat our dogs should carry. It was once said, you could hunt with your Gordon on Saturday and show him in the ring on Sunday.  That’s definitely harder to do today.  I truly believe you can still finish a championship on a well constructed dog, under knowledgable judges, without an over abundance of coat.

Impressions1
Photo by Ben Perez, 2016 GSCA National Specialty

Once you move to the specials ring, the game is stepped up a bit.  To compete in today’s groups, coat and presentation become big factors.  I believe it would be very hard to pull out group placements and specialty breed wins without it.  It’s become an expectation.  The dogs who are truly competitive at this level, generally have more than coat and meticulous grooming going for them.  I urge breeders and newcomers to politely seek out opportunities to examine as many of these dogs as possible.  I will bet you find “hidden” attributes you didn’t know were there.  That said, if you bought a dog with an abundance of coat for hunting, but you also want to show him in the breed ring, be prepared to take measures to protect the coat or make choices as to which endeavors you wish to pursue and when.  I don’t think we will be returning to the way things were in the sixties or seventies.

Impressions4
Photo by Ben Perez, 2016 GSCA National Specialty

 

I really enjoyed seeing many of you at the National.  The committee did a great job and I enjoyed the low key atmosphere.  It was so nice, as it always is, to see the dogs.  Thank you to all who participated in the hands on breeders education and a special thank you to those who shared their dogs with us.  Without you, it would not have been a success.

Barbara Manson, Stoughton  WI

Photographs by Ben Perez are shared for your viewing pleasure and are not intended to illustrate any specific point in this article.

Impressions3
Photo by Ben Perez, 2016 GSCA National Specialty

 

Breeding, Health & Genetics

Death by a Thousand Health Tests

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Food for thought is always a good thing, at least in my world, it keeps my mind open to new ideas. As I’ve aged I’ve found it’s ever more important not to get stuck in my ways and thinking about what other people have to say on a topic keeps me out of ruts.  So when I read the article I’m sharing with you today about health testing, I found myself thinking. Now, a word of warning, some of my close friends would tell you, “Sally’s thinking takes some rather weird detours now and again, so when she says “I was thinking” you might wanna run for cover!”

We all talk about being a responsible breeder, and of course, we consider a part of that responsibility to be health testing of the parents. Now mind you, I’m getting to that place where I’m almost old as dirt, so I’m one of those breeders who started in the game long before the majority of the health tests of today were available. While I’m all for health testing to gain knowledge of what is in the genes I’m about to mix together, I’m also one of those breeders who will tell you to use a good ole dose of common sense when breeding. While I’d never throw health testing to the side, I am also realizing that as the population of Gordon Setters declines, so follows our number of breeding options. This is a big conundrum we face folks, and it will take dedication, smart decisions and some good old common sense to preserve the best of our breed.

Sally Gift, AZ              Photograph by Susan Roy Nelson, WY

With that said, I don’t know as I agree with everything in this article, but I do know it will give you some food for thought so I’m sharing, for your reading and thinking pleasure.  If you’d like to share your thoughts after reading this feel free to use the comment section!

Breeder On The Edge

Death From a Thousand Health Tests by Amanda Kelly

AUTHOR:  A dedicated hobby breeder in a terminally rare breed, Amanda Kelly perpetually finds herself on the edge of everything from ecstasy to bankruptcy, quitting and insanity.

I had a really interesting conversation with a geneticist the other day that got me thinking: science is offering us more and more great ways to evaluate the health of our dogs…but when does enough turn into too much? When do we cross the threshold from helpful information to complete paralysis? Or outright bankruptcy? How do we avoid both?

Prioritization
The test we were discussing is quite a new one in my breed (Toy Manchester Terriers). It is for a condition called Xanthinuria that causes dogs to form a very rare form of kidney stone. There have only been three clinically affected dogs that I am aware of (full disclosure: we bred one). After encountering the issue, a fellow breeder did a little digging and discovered that a marker associated with the condition in humans worked for our breed as well. Kudos to her for being proactive and finding out more! The American and Canadian breed clubs helped proof the test and voila, it is now available commercially at quite a reasonable cost.

When I looked at dogs in my own breeding program that came up as carriers however, I was surprised as I would have expected more of our puppies to have or be forming stones than was the case.  So, what does that say about the disease? Do all affected puppies form stones? If not, what is the rate?  I found the answers to those Qs simultaneously helpful and troubling.

Apparently, current thinking is that approximately 50% of males with two copies of the mutation form stones or have associated kidney issues, while very few females with the same status have a problem (likely because they do a better job of emptying their bladders). Now, these are just rough estimates because the disease as a whole is rare and hasn’t been extensively studied, but it does raise an important question: what are we as breeders to do with this information and associated results of the genetic test?

The Jigsaw
The simple fact is that the more tests we have, the more pieces of info we have to try and reconcile when planning a breeding. At present, Toy Manchester breeders as a group are variously clearing things like hips, patellas, eyes, thyroid, and hearts plus DNA testing for von Willebrand’s Disease, and, now, potentially xanthinuria. That’s 7 tests, some with questionable value based on anecdotal and surveillance evidence, if we’re being honest. We’re also actively working to identify a test for juvenile cardiomyopathy.

The end result of all of that testing is a ton of information, which is great from the perspective of evaluating the health of individual dogs but also creates a number of very real problems for breeders in areas like liability, reputation and cost.

In the past, these factors were certainly in play but their effects were somewhat muted. Breeders worked for years to learn about their breed and their lines so they could make informed decisions and minimize the risk of producing issues. Health tests initially concentrated on measuring phenotype as an indicator and we worked with what we had. The important thing was that we could confidently tell puppy buyers we had done everything possible to produce healthy, happy puppies and if a problem appeared we were solid in the knowledge we had used all available tools to their best advantage.

Enter the genetic test. In my breed, the first one was for von Willebrand’s Disease (a blood clotting disorder). For years this disease was monitored by assay testing that measured the actual amount of the specific type of clotting factor in the blood and projected genetic status based on corresponding ranges. It was a pain to do but everyone muddled through as it was one of the few standard health tests most breeders did in the 1980s and 90s. When the genetic marker was identified, some breeders lost their ever loving minds. Dozens of valuable dogs were promptly spayed and neutered while breeders across North America began making pronunciations about “never” breeding a carrier even to a clear.

There’s no question, needless damage was done to the gene pool — especially when you consider there had never been a documented case of a Manchester actually bleeding out because it was vWD affected (at least not one I am aware of). Eventually breeders learned how to work with the DNA results and things calmed down. Our new test allowed us to easily avoid producing “affected” puppies (i.e., a dog with two copies of the gene, not necessarily clinically affected) and, regardless of the actual effects of the condition itself, doing so quickly became “right” and “just”.  It was an approach we ourselves endorsed and followed because, after all, “responsible breeders” test.

And thus, the line in the sand was drawn. It’s a line we in the dog community drew ourselves and it’s one most of us dare not cross.

Unlimited Liability
The scientific advancements that brought us more genetic tests took place against an active backdrop that included the rise of animal rights, increasing anthropomorphization of pets, emergence of puppy lemon laws, and the advent of social media. Now, it may seem odd to bring those factors into a discussion of genetic testing, but they each play a very important role in describing the environment within which we are working. An environment that values reputation above all else and that pits breeding decisions against financial liability in a way many breeders don’t consider.

Any breeder with two licks of sense knows that when it comes to breeding dogs, the most important possession you have — more important than any ribbon you may ever win — is your reputation. Your reputation affects everything you do, from access to stud dogs and puppies to demand for same. In a subjective sport like ours, it can even affect your ability to succeed in the show ring.

Protecting, fostering and growing a reputation can become all-consuming. Let’s cut to the chase here: We’re operating in an environment that can make a competition out of anything — which is why sometimes reputation management, and by extension health testing, becomes as much about one upmanship and moral superiority as it is the well-being of the dogs in question. That probably explains why many of the tests done in my breed are done by rote…because they are available, not because we have objectively identified a need for them. Not because we have established that rates of thyroid problems or eye issues, for example, are any higher in our breed than in the general dog population. No, we do them because we can and because we feel (tell one another?) that we should. And why is that? It’s because we have established as fact within our community that good breeders test and bad breeders don’t. So, we all work extra hard to make sure our conduct is above reproach.

That core belief is just as strong outside of the dog community, where we have worked hard to battle animal rights messaging by establishing health testing as a key feature differentiating responsible breeders from backyard breeders. And it’s a great message — easy to understand and easy for the public to actively measure when they are talking to breeders. The trouble is, that message comes pre-loaded with expectations we can never live up to. Expectations that if you buy from a good breeder your dog will never ever have health issues. That health tested parents won’t produce problems. That responsible breeders can be God.

And therein lies the problem. The more health testing we do, the bigger the gap grows between public expectations and the reality of what we can deliver…and with it, our financial liability. Because hey, don’t forget, in addition to health testing, responsible breeders also guarantee their puppies. Whether through provision of a replacement puppy or return of purchase funds, those guarantees do carry financial risk and can’t be dismissed at the best of times and even less so as puppy lemon laws increasingly make puppy health a legal matter. So, tell me…how do you think small claims court would view a breeder that knowingly produces a problem? Or one that unknowingly produces one because they failed to use the tests available? It’s a perfect catch 22 in the making.

Risk Reduction
It’s a simple axiom that the more health testing available, the less we talk about what we’re trying to avoid producing and the more we talk about what we are willing to risk producing. There isn’t a perfect dog out there and every biological organism possesses deleterious genes for something, regardless of whether we can test for it or not.  The more tests available, the more complicated planning breedings becomes because we all naturally want to avoid the chances of producing any problem at all.  But is that a realistic goal?

What did I say we were up to in my breed – seven tests? Eight? Heck, even I lose track sometimes. And all of these tests in an era when the number of puppies being produced continues to drop at an alarming rate. Under 200 Toy and Standard Manchester Terriers “combined” were produced in North America last year, so I’m sure you can image how difficult it might be to match test results for potential breedings (particularly if we’re testing for everything under the sun). Or what the costs of doing those breedings might be as we look further and further afield, let alone the relative cost of doing the health screening to begin with in a breed with relatively small litter sizes and low purchase prices. The financials would rock your world and have you questioning my sanity, so we won’t go there other than to say red is a better quality in a new coat than a ledger (but I digress…).

I asked a few researchers and vets what they felt breeders should do with test results when there are many to consider.  The consistent response was that we need to prioritize — and that’s a completely reasonable thing for a scientist to say…and a very difficult thing for a devoted dog breeder to actually do.

Never mind the costs, appearance or liability — I genuinely don’t want to be responsible through conscious decision for producing a sick puppy. It is one thing to employ testing, tools and techniques to theoretically reduce disease and quite another to look at a plethora of results and say “This one I can live with.”

And what happens once the die is cast?  If we use Xanthinuria as an example, I could choose to breed two carriers together and test all of the puppies…but then what? Sure, knowing a puppy has two copies of the gene and is at higher risk of forming stones will be helpful to an owner who could keep the dog on a low purine diet and perhaps avoid issues altogether…but could I sell a puppy like that? For how much? Would anyone take it if I was giving it away? What level of financial responsibility do I hold if it does develop an issue two, five or 10 years down the road? What if there are multiple puppies with two copies of the gene in the litter?

And that, ladies and gentlemen, is the ethical dilemma of the future.  Perhaps we in smaller, rarer breeds are dealing with it sooner, but it is a dilemma I truly believe every breed and breeder will face at some point.  It has the potential to be absolutely paralyzing as we seek to do the right thing in a world where that is increasingly less black and white than it seemed a few short years ago.

I don’t know exactly how we can or should approach it — perhaps I’m hoping you’ll be able to tell me. I suspect that monitoring of actual breed health through health surveys and breeders sharing information on what they are seeing will be increasingly important if we wish to prioritize according to real information. And I do know that one of the things we absolutely must do is change how we discuss health testing. The way we talk about each other (oh Lordy, put a star next to that one!) and to each other as well as how we portray ourselves to the public. Just as important, we have to think about health tests and results holistically in the context of our breed and gene pool. In our rush to erase problems through testing, we are shown again and again that the devil we don’t know is often worse than the devil we can test for.

What To Do?
This article isn’t intended to form the cornerstone of a campaign against health testing. Far from it. I truly believe we need to use the tools available to us, particularly if they are able to help us avoid devastating issues facing our dogs and puppies. In fact, I and others in my breed have worked hard for more than a decade to see a genetic test developed for juvenile cardiomyopathy because it is a brutal, deadly disease and I want all of us to have a tool that will allow us to make informed choices and stop guessing at how to avoid it.

But I’m also a realist. Health management is a tough nut to crack even for trained geneticists let alone the average breeder doing their best to navigate an increasingly complex and technical landscape. Giving us the test results is the easy part, it seems — figuring out what to do with them is our next great challenge.

Breeding, Catch All, Whelping

Free Ad Space for Gordon Puppies, Adults, Litters

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As the Gordon Setter Expert audience has grown tremendously, so has the amount of email that I get from people who are searching for quality Gordon Setters from responsible breeders.

To simplify the process where I connect those who are searching for Gordon Setters, with those who are searching for good homes, I’ve created this FREE listing – that’s right, you may advertise to sell your Gordon Setters for free, right here on this site! If you have a puppy, a litter, an adult or are planning a breeding this free service is the perfect value! I’ll be happy to include your photos and pedigree too.

I’ve set a few parameters to ensure I am working with responsible breeders who are invested in the preservation and promotion of the Gordon Setter breed, and you’ll find the rules and restrictions regarding this listing service by visiting the pages below.

Don’t worry about losing this message, just remember that you can go to the Gordon Setter Expert “Home” page any day and simply click the header at the top of the page that reads “Place an Ad – Puppy, Adult, Planned breeding”.

Want to see what your ad might look like? Click here

Place an Ad – Puppy, Adult, Planned Breeding

Gordon Setter Future Litter (Planned Breeding) 

Gordon Setter Puppies

Gordon Setter Adult

I’m certainly hoping Gordon Setter breeders and owners will find this service helpful, that’s all I’m here for, to help!

Don’t forget – you can also list your Stud Dogs here for free!

Sally Gift, Mesa AZ

Photograph by Laurie Ward

Breed Standard, Dog Shows

The Hands On Experience

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GSCA Breeder Education – 2016 GSCA National Specialty

By Sally Gift

To begin let’s start with excerpts from

Looking at Dogs in a Positive Light When Judging From the March 2015 issue of Dogs in Review magazine.

By Kathy Lorentzen

Positive and clearly explained judging can only be good for both judges and breeders, and for our breeds as well.

Have you ever noticed how easy it is for people to look at a dog and immediately point out what they don’t like about that dog? I think most often the first comments made by many people about a dog are negative. We hear an awful lot of “I don’t like” in conversations about dogs.

Probably we are all guilty of falling into the trap of finding fault, both as breeders and as judges, because finding fault is easier than finding virtue. Common faults are easily seen and identified by almost everyone, while breed-specific virtues can only be seen and appreciated by those who truly understand the breed they are looking at…Even judges (sic Breeders) with years of experience were tongue tied when forced to discuss their placements by pointing out only the virtues of each dog. They all wanted to fall back into the “I don’t like” syndrome.

…The positive mindset is not only important for judges but for breeders as well. How many times have I asked a fellow breeder, “What do you think of that dog?” only to have the first sentence come back starting with, “Well, I don’t like…” After my years of learning about positive judging and critiquing, my immediate reaction is to say, “But I want to know what you do like about that dog.” The look I get is generally priceless, but my question usually results in a thoughtful discussion of the virtue of the dog and a learning experience for both of us.

Not everyone will see the exact same virtues in every dog, and not everyone will place the same priorities on those virtues. That is why different dogs win on different days, and when the judging is positive and can be clearly explained, then no one is wrong. But regardless of differing viewpoints and priorities, striving to see dogs in a positive light can only be good for both judges and breeders, and for our breeds as well.

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In forming our concept of the Hands On experience, and in addition to focusing on judging dogs positively, we also wanted to encourage breeders and exhibitors to take the time to put their hands on dogs owned and bred by others; to learn how to feel breed specific qualities to recognize correct structure (breed type), to learn a variety of ideas and concepts from others, and to learn how to see good qualities in all dogs, our own as well as those owned by others – to learn how to develop an unbiased eye.

Now let’s move on to highlights from the Hands On experience!

I can’t possibly write about all the topics we covered, nor all the positives of the dogs presented for exam. But if I haven’t covered a topic or a point that you want to see shared here please offer that in the comment section of this article.

The Hands On experience was open forum, and participants were encouraged to come and go at will, so the group size and the participants fluctuated throughout the program. Some brought dogs who were stacked in front of the group while other participants went over those dogs, the Hands On part. Then, those who examined were asked to share their view of the positive qualities they found on the dog they examined. Discussion about the positives followed with the group at large joining the talk. While committee members, Barb Manson, Peggy Nowak and I moderated to keep things on track, the teachers here were actually the participants, the many breeders and exhibitors who shared their dogs, views, and experience. The Hands On experience lead to many various, thought provoking and enlightening discussions. The participants and their dogs were the shining stars of the experience, and we thank each and every one of you for making this one of the best GSCA Breeder Education events. We have heard a magnitude of positive feedback, and what we heard most often was indeed “best Breeder Education program ever” and “let’s do it again”!

Breeders ed6 2016
Photo by Ben Perez

 

Topics that were covered during the experience

Esther Joseph (Australia) shared many interesting points about length of body and the length and structure of the rib cage. She noted that when compared to other countries, the American Kennel Club (AKC) Gordon Setter Standard, is the only standard to to call for a length approximately to equal height, interpreted by many to mean we seek a “a square dog”.

  • AKC Standard – Proportion: The distance from the forechest to the back of the thigh is approximately equal the height from the ground to the withers.
  • Australian National Kennel Council (ANKC) Standard – Body: Moderate length.

One of the key takeaways that I would mention is the wording in the AKC standard, wording that says approximately equal, as this wording gives the Gordon room for sufficient length of body to allow for the driving stride he will exhibit if properly angled front and rear. A dog whose body is too short for the angulation of his rear can not move properly. If we were to breed for a completely square Gordon we would need to breed that dog with less angulation in the rear, so his rear stride does not interfere with his front. Perhaps we need to focus on the standard saying approximately equal and eliminate the word square from our lingo?

The AKC standard says Gordon Setter movement should be: A bold, strong, driving free swinging gait…The hindquarters reach well forward and stretch far back, enabling the stride to be long and the drive powerful. If, for example, a Gordon moves wide in the rear, or perhaps he crabs, we might consider that one of the causes could be that Gordon has too much rear angulation for the length of the body. Is this dog then too short in length (too square)?

(NOTE – as a question was raised, I did confirm the information I gave you regarding how to measure the dog’s length. I was correct, it is measured from the point of the forechest and never from the point on the shoulder joint)

Another discussion ensued on proper length, depth, and spring of rib. Here again Esther opened the chat and spoke in detail about the length of the rib cage and it’s importance for the protection of the Gordon’s vital organs (heart and lungs) when hunting in dense brush and brambles. To completely shield those organs the ribcage must be long from front to back, and we should measure this not simply by looking at the length from the side view of the dog, but also by reaching down under the dog to note how how far back the sternum extends. (The sternum being the floor of the chest, where the ribs meet underneath the dog.)  The Gordon Setter needs not only his prominent forechest (for proper muscle attachment to provide reach) but also good length of the ribcage; a sternum whose length extends it’s boney protection to completely cover sensitive organs. A ribcage and which allows for the lung capacity he needs by it’s spring as well as depth for working in harsh terrain.

Barbara Manson began a discussion about short hocks by demonstrating that good quality on her dog. This  led into a more in depth conversation among the group about the complete rear assembly, angulation, length of hock and sickle hocks. When viewing rear angulation we’d start at the highest point, the femur (think upper thigh) which has always been considered as the longest bone in the dog’s anatomy. The tibia and fibula (second thigh) should be second in length to the femur, and are attached to the hock which should be the shortest in this group of leg bones that contribute to rear angulation. Simple so far, right?

Standing around at rest (as opposed to lusting after a hot smelling bitch which brings every hot blooded dog up on his toes) a well built dog will naturally stand with the rear foot in a somewhat perpendicular line on the ground, right under the boney protuberance that ends at the point of the buttocks.  Just like humans, dogs stand around with their feet almost directly under their butts. Why? Because that’s the dog’s column of support. So, if the second thigh (tibia and fibula) is longer than the upper thigh (femur), opposite the normal length of these bones, the only way the dog can reach his column of support is if the hock is long enough to get the foot where it needs to be – underneath the dogs butt. Proper ratio of length between upper thigh and lower thigh gives us the shorter hock we expect on our Gordon Setter. To sum it, a Gordon needs to have an upper thigh (femur) that is longer than the lower thigh (tibia and fibula), ending with a hock that is shorter than both of those bones.  As a general rule, the genes that control the length of one bone are often linked to the genes that control the length of the corresponding bones so Mother Nature provides compensation when the ratio in the length of these bones gets out of whack, grow a lower thigh that’s too long for the upper thigh and Mother Nature will give you a longer hock to compensate.

Standing around ringside, looking at dogs standing in a relaxed state, the well put together dogs will be standing with their rear feet underneath the back half of the pelvis and their hocks slightly sloping – we should be able to see light between the ground and the entire length of dog’s hock. If a dog is standing with his hocks nearly flat to the ground, odds are excellent that we are looking at excessive angulation (a lower thigh that is longer than the femur).

Sickle hocks are a result of these over angulated rears. For me, sickle hocks are easily seen on the backward swing of the rear leg during movement. Instead of the joint between the lower thigh and the hock opening up into a nearly straight extended line, where the pads on the bottom of the foot end in a position that is nearly straight up (or reaching toward the sky), the sickle hock, due to the imbalanced length of the bones, at fullest rearward extension ends in a shape resembling a sickle – slightly curved instead of fully extended. No glimpse of the sky for the pads on these feet. The rear movement on the sickle hocked dog looks like the swinging of an old fashioned sickle when viewing the sickle from the side.

Our group also spent a bit of time discussing feet. We’re not going to cover all of that discussion here as this article has grown quite long. I did want to mention that I remember a brief conversation around the use of the term “cat foot”. Perhaps I remember wrong but I thought I heard someone say that “cat foot” no longer appeared in our standard.  You were right, cat foot isn’t exactly right, but a reference to cat does appear. The standard says “Feet catlike in shape”. 

I’m splitting this report into sections as it’s growing long, keep an eye out for Part II – The 2016 National Specialty Hands On experience in a future issue. In Part II I’ll share other discussions we held on topics like the width of jaw, angle of croup, block on block heads and vitiglio.

Sally Gift, Mesa AZ  GSCA Breeder Education Committee Chair

Photos by Ben Perez

A slide show of random photos from the BOB class at the ’16 GSCA National Specialty courtesy of Ben Perez. We’ll be sharing more of these in future articles. Thanks Ben!

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Catch All

An Eye On Legislation – April 2016

7 Comments
By Charles Kushell – GSCA Legislative Liaison
“Let’s see what our elected elves have been up to this past month.  A few items to note during this silly political season; this may be as much fun to watch as the runup to the 1912 convention season must have been.
CT/MA:  This from our friends at the CFD/MFD regarding a dangerous bill SB-288 before the CT Assemble that seeks to impose onerous and ill-considered and unnecessary new restrictions on pet owners and kennel operators.  This mess is the perfect example of the cancerous nature of “committees and task forces” which even when killed by the toxic chemo of iron-clad sunset date requirements, simply refuse to die, and like zombies, keep coming back from the dead.  And so it is here; a “task force” under legislative mandate to expire…that’s as in DIE AND DON’T COME BACK…has not only NOT died, but is trying to re-assert itself into permanence by attaching a new version of an already-bad bill.  https://www.cga.ct.gov/asp/cgabillstatus/cgabillstatus.asp?selBillType=Bill&bill_num=SB-228.  Folks also need to pay attention to HB5344 which seeks to establish some bizarre and incomprehensible “non-economic damages” recovery aspect of pet damage cases and to establish court-appointed “advocates” court pet-related cases.  God help us, just what we need.  All CT dog owners should call their state senators with a strong demand to make this idiocy go away once and for all.  We wish you luck with this crowd.
CA:  You simply knew that CA would be in this column; the state of perennial legislative insanity.  This time it’s the city of Colton.  Don’t feel bad, I live in SoCal and still had to look it up.  If nothing else, it proves that systemic lunacy isn’t limited to Sacramento.  These geniuses must be living in a time-warp; the City Council has decided to push a “must neuter” ordnance that fails to exempt legit breeders and seeks to limit dogs to 10 per HH.  Anyone living in this paradise should contact these poor unfortunates and inform them that must-neuter laws are uniformly rejected by communities operating in the 21st Century.
IL:  You know, for a state that is bankrupt, failing to pay its bills and cannot meet its pension obligations, you’d think State legislators could find more pressing things to do than make up bad pet laws.  Apparently not.  Such a twisted sense of priorities has begotten  HB4443 which seeks to establish such blatantly un-Constitutional niceties as warrant arrests in cases of alleged animal “abuse”…even when no evidence has been provided.  Essentially, your neighbor could theoretically hear your dog complaining about your Dremel-ing his toenails, turn you in and IL authorities would be able to arrest you, seize your dogs, charge you for their board and provide immunity from the exact same type of complaint of cruelty!!!.  ALL IL pet owners need to contact their State reps to express their horror and outrage at this prospective bill.  Hard to believe.
MO:  Here’s a chance to call your State rep and urge their support of HB1811, which seeks (mercifully) to ban any local MO community from writing, passing or attempting to enforce breed-specific legislation of any kind.  Similar to the AKC-sponsored white-label legislative proposal, this puts MO right at the forefront of state legislative bodies who have done their homework, resisted the bleating of the “animal-rights” crowd, and seek to establish fair and sane laws.  Bully for them.  Call and urge them to see it through.
IA:  Delighted to report that through the combined efforts of local breeders, clubs and the AKC, the legislature of IA has hung it up for the year (why doesn’t the US Congress try the same thing?) and resisted passing ANY of some of the truly horrible bills (reported here earlier) that had crawled before it.  Good on them and congrats to the good people of the dog community there and to the AKC for their good work.  Would that other states pay attention.
FL:  This time, heads up Broward residents.  As you’re painfully aware, you’re under draconian breeder laws there.  It gets worse.  The locals are considering new pile-on amendments to an already horrid law that would make you agree as a condition of your license to submit to warrantless searches of your home.  Apparently, these idiots are unfamiliar with the Fourth Amendment of the US Constitution forbidding exactly this kind of law.  Get off your rears, Broward breeders (this assumes there are any left) and get on the horn with the Broward Cty Commissioners and have at it.  Insane.
Ok, enough for now.  And as ‘ol H.L always instructed us, “A good politician is quite as unthinkable as an honest burglar.”
Amen.
c”
Photographs courtesy of Jim Thacker – GSCA National/Midwest Specialties 2016