Bobtail data from qualified sources

In this page I do not hesitate in saying that all the data is from gathered sources which I have collated over the years most from University papers .

p://www.border-wars.com/2011/03/lethal-semi-dominant-bobtail.html

Semi-dominant alleles are those that are less potent in heterozygous form (one copy) than they are in homozygous form (two copies), but which are potent enough to show a difference in phenotype from the wild-type allele (no copy). Recessive alleles show no difference with only one copy versus zero copies, and fully dominant alleles look the same with one copy as with two.

A lethal allele is a variation of a gene that will eventually cause death, perhaps even a failure of conception or birth

Such is the case with the most common allele which results in a natural bobtail. This gene has been documented in a number of breeds including: the Australian Shepherd, Austrian Pinscher, Australian Stumpy Tail Cattle Dog, Braque du Bourbonnais / Bourbonnais Pointer, Brazilian Terrier, Brittany Spaniel, Croatian Sheepdog, Danish Swedish Farmdog, Jack Russell Terrier, Karelian Bear Dog, Mudi, Polish Lowland Sheepdog, Pyrenean Shepherd, Braque Francais / Savoy Sheepdog, Schipperke, Spanish Water Dog, Swedish Vallhund, and the Pembroke Welsh Corgi. It has also been intentionally introduced into the Boxer to keep the look of a docked tail in countries that have outlawed docking.

Congenitally short-tailed dogs are present in many breeds; however, the causative mutation located in the T-box transcription factor T gene (C189G) had only been described in the bobtailed Pembroke Welsh Corgis. We investigated here the presence of the T gene mutation in 23 other breeds (360 dogs, including 156 natural short tailed) in which natural bobtailed dogs exist. In the 17 breeds in which the C189G mutation was observed, there was a perfect correlation between this mutation and the short-tail phenotype. However, 6 breeds did not carry the known substitution or any other mutations in the T gene coding regions. No dogs were found to be homozygous for the C189G mutation, suggesting that the homozygous condition is lethal. In order to study the effect of the T gene mutation on litter size, we compared the number of puppies born from short-tailed parents to that born from long-tailed parents. In the Swedish Vallhund breed, we observed a 29% decrease in the litter size when both parents were short tailed.

The Boston Terrier, English Bulldog, King Charles Spaniel, Minitaure Schnauzer, Parson Russel Terrier, and Rottweiler exhibit natural bobtails but do not carry the C189G mutation, and the following breeds have not been tested to confirm what mutation causes their bobtails: the French Bulldog, McNab, Miniature Fox Terrier, Old English Sheepdog, Rat Terrier, and Tenterfield Terrier

Like Merle and one of the Hairless alleles, the C189G mutation is considered semi-dominant and lethal, but unlike those other two, there has not been scientific observation of negative health effects (other than the lack of a tail obviously) in dogs with only a single copy:

In contrast with homozygous, heterozygous bobtailed dogs have not been reported to manifest any other abnormalities (Indrebø et al. 2007).

While some breeders are claiming that the bobtail gene is also superior to the other known lethal semi-dominants in that it does not produce live homozygotes (“it only hurts eggs”), there are documented double bobtails that have been born with severe deformities:

Recently, Pembroke Welsh Corgi puppies with severe anatomical defects having the homozygous mutation have been characterized. These puppies lacked tails, manifested anorectal atresia with severe alterations in the posterior lumbar region and spine, and had a failure to thrive (Indrebø et al. 2007)


o beyond the ethical implications of killing embryos (out of sight, out of mind for most breeders), the double bobtail allele can produce profoundly crippled live births.  The ethics of this are a bit more problematic.  Although given that other scientific inquiries were unable to account for surviving double bobtails, it’s likely that the homozygous form is particularly lethal resulting in only a small percent of surviving puppies.  Unlike some theories that these fatalities have little or no effect on litter size (the assumption being that the embryo would fail early enough for another non-homozygote to thrive in its place), the above referenced study did show a nearly 30% reduction in bobtail x bobtail litters.  Sadly, they didn’t report on bobtail x tail fertility.

Two carriers for the Bobtail gene will produce embryos in the ratio of 1:2:1, resulting in a phenotype of 1:3 tail to no-tail (25%). But since the homozygous no-tail state is almost universally fatal early in pregnancy, we observe that a third of live births in breeds with the C189G mutation will be normal with tails
Without a healthy example of a double bobtail, the most concentrated we can breed to maximize the number of bobtail puppies is Carrier x Carrier, as documented in the diagram above.  The lack of a healthy homozygote for bobtail gene means that this mutation will never be able to provide a completely bobtail strain that breeds true.  There will always be a 33% undesirable overhead (dogs with tails) in any bobtail breeding plan.  If we chose to consider the lethal homozygotes as well, there’s a 50% undesirable overhead in the effort to breed bobtail dogs with this gene.  I think that’s a significant enough percent to question the ethics and efficacy of a genetic solution versus a surgical one.

Adorable Corgis provided courtesy of Cartoonize My Pet.

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ogs[edit]

A mutation in a gene called the T-box transcription factor T gene (C189G) accounts for natural bobtails in 17 of 23 dog breeds studied, but not in another 6 dog breeds, for which the genetic mechanism is yet to be determined.[2]

Natural bobtail dog breeds with C189G mutation:

Natural bobtail dog breeds without C189G mutation:

Dog breeds into which the C189G mutation has been introduced by cross-breeding:

Dog breeds where natural bobtails have not yet been tested for C189G mutation:

References[edit]

  1. Jump up^ The Fantastic Account of Dr Bruce Cattanach’s Bobtail Boxers Virginia Zurflieh, boxerunderground.com, Oct 1998.
    1. Jump up^ Hytönen et al (2008), “Ancestral T-Box mutation is present in many, but not all, short-tailed dog breeds”, Journal of Heredity, Advance Access published online on October 14, 2008,doi:10.1093/jhered/esn085 [1]

External links[edit]

UNIVERSITY OF CALIFORNIA

https://www.vgl.ucdavis.edu/services/Bobtail.php

Natural Bobtail

Introduction

Natural bobtail (NBT) is a naturally occurring mutation in the T-box gene resulting in a shortened tail. The mutation is inherited in an autosomal dominant fashion with both sexes being equally affected.  This mode of inheritance means that presence of one copy of the mutant gene will produce the bobbed tail phenotype in males and females. The length of the bobbed tail is variable and under the influence of other as yet undetermined genetic factors that cause some NBT individuals to have nearly full-length tails while others may have virtually no tail.  While heterozygous individuals (possessing one normal and one affected T gene) have shortened tails, data suggest that the homozygous condition (possessing two copies of the affected gene) is lethal in utero. Breeding of two carriers is predicted to produce 25% homozygous affected offspring thus a 25% reduction in litter size.

Genetic testing is recommended to verify and validate the natural bobtail status of dogs, especially if docking is allowed, and to help with breeding pair selection to eliminate the risk of reduced litter size. Testing is recommended for: Australian Shepherd, Austrian Pinscher, Australian Cattle Dog, Bourbonnais Pointer, Brazilian Terrier, Brittany Spaniel, Catahoula Leopard Dog, Croatian Sheepdog, Danish/Swedish Farmdog, Jack Russell Terrier, Karelian Bear Dog, McNab, Mudi, Pembroke Welsh Corgi, Polish Lowland Sheepdog, Pyrenean Shepherd, Savoy Sheepdog, Schipperke, Spanish Waterdog, Swedish Vallhund.

The VGL offers a test for Natural Bobtail to assist owners and breeders in identifying dogs that have this trait. The test uses DNA collected from buccal (cheek) swabs, thus avoiding blood sample collection.

ORDER TEST KITS | PRICE LIST
Allow 2-6 business days for results.

Results reported as:

Test ResultNatural Bobtail
N/NNormal – no copies of the NBT mutation
N/BTNatural bobtail – 1 copy of the NBT mutation
BT/BTNatural bobtail – 2 copies of the NBT mutation*

* Result unlikely to occur for live dogs; NBT is considered a homozygous lethal in utero.


Reference:
Haworth K, Putt W, Cattanach B, Breen M, Binns M, Lingaas F, Edwards YH. 2001 Canine homolog of the T-box transcription factor T; failure of the protein to bind to its DNA target leads to a short-tail phenotype. Mamm Genome. 12:212-218.

Hytönen MK1, Grall A, Hédan B, Dréano S, Seguin SJ, Delattre D, Thomas A, Galibert F, Paulin L, Lohi H, Sainio K, André C. 2009. Ancestral T-box mutation is present in many, but not all, short-tailed dog breeds. J Hered. Mar-Apr;100(2):236-40.

http://www.ncbi.nlm.nih.gov/pubmed/1885437

Send to:

J Hered. 2009 Mar-Apr;100(2):236-40. doi: 10.1093/jhered/esn085. Epub 2008 Oct 14.

Ancestral T-box mutation is present in many, but not all, short-tailed dog breeds.

Hytönen MK1Grall AHédan BDréano SSeguin SJDelattre DThomas AGalibert FPaulin LLohi HSainio KAndré C.

Author information

MID:

http://jhered.oxfordjournals.org/content/100/2/236.long

  1. Marjo K. Hytönen*
  2. Anaïs Grall*
  3. Benoît Hédan
  4. Stéphane Dréano
  5. Samuel J. Seguin,
  6. Delphine Delattre
  7. Anne Thomas
  8. Francis Galibert
  9. Lars Paulin
  10. Hannes Lohi
  11. Kirsi Sainioand 
  12. Catherine André

+Author Affiliations 1.     From the Medical Biochemistry and Developmental Biology, Institute of Biomedicine, University of Helsinki, PO Box 63, 00014 Helsinki, Finland (Hytönen and Sainio); the Institut de Génétique et Développement, UMR 6061 CNRS/Université de Rennes1, Faculté de Médecine, 35043 Rennes Cedex, France (Grall, Hédan, Dréano, Seguin, Galibert, and André); the Antagene, Research and analysis laboratory in animal genomics, 2 allée des séquoias, 69760 Limonest, France (Delattre and Thomas); the DNA Sequencing Laboratory, Institute of Biotechnology, University of Helsinki, PO Box 56, 00014 Helsinki, Finland (Paulin); and the Department of Medical Genetics and Department of Basic Veterinary Sciences, University of Helsinki and the Folkhälsan Institute of Genetics, Department of Molecular Genetics, PO Box 63, 00014 Helsinki, Finland (Hytönen and Lohi)

  1. Address correspondence to Marjo K. Hytönen at the address above, or e-mail:marjo.hytonen@helsinki.fi.
  2. Received April 17, 2008.
  3. Revision received September 10, 2008.
  4. Accepted September 15, 2008.

Next Section

Abstract

Dogs differ greatly in their morphological characteristics including various tail phenotypes. Congenitally short-tailed dogs are present in many breeds; however, the causative mutation located in the T-box transcription factor T gene (C189G) had only been described in the bobtailed Pembroke Welsh Corgis. We investigated here the presence of the T gene mutation in 23 other breeds (360 dogs, including 156 natural short tailed) in which natural bobtailed dogs exist. In the 17 breeds in which the C189G mutation was observed, there was a perfect correlation between this mutation and the short-tail phenotype. However, 6 breeds did not carry the known substitution or any other mutations in the T gene coding regions. No dogs were found to be homozygous for the C189G mutation, suggesting that the homozygous condition is lethal. In order to study the effect of the T gene mutation on litter size, we compared the number of puppies born from short-tailed parents to that born from long-tailed parents. In the Swedish Vallhund breed, we observed a 29% decrease in the litter size when both parents were short tailed. Given that the Tgene mutation is not present in all breeds of short-tailed dog, there must be yet other genetic factors affecting tail phenotypes to be discovered.

Key words

Dogs have become important models for genetic studies due to their extensive phenotypic variation, unique breed structure, as well as available genome sequence and genetic tools (Sutter and Ostrander 2004Lindblad-Toh et al. 2005Starkey et al. 2005Tsai et al. 2007). Selective breeding has enriched many breed-specific morphological characteristics including tail length. Tail length depends on the number of the caudal vertebrae, which can vary significantly between individuals. Several dog breeds show very short tails (brachyury) or even complete absence of the tail vertebrae (anury) as illustrated in Figure 1. A genetic cause of short-tail phenotype has been identified in Pembroke Welsh Corgis (Haworth et al. 2001). The C189G mutation in exon 1 of the T-box transcription factor T gene affects the DNA-binding property of the T protein resulting in the bobtail phenotype. Pembroke Welsh Corgis heterozygous for the C189G mutation have short tails, and this mutation is thought to cause embryonic lethality in homozygotes (Haworth et al. 2001Indrebø et al. 2007). T gene mutations in mouse cause early embryonic lethality and abnormalities in the development of mesodermal tissues, including the tail and spine, thus suggesting an essential role for the T gene during mammalian development (Wilson et al. 1995). In addition to the T gene, mutations in other genes like Pax1 and Wnt-3a have been associated with tail development in mouse (Greco et al. 1996Wilm et al. 1998).

View larger version:

Figure 1

Illustration of Bourbonnais Pointer dogs showing a tailless (anury) phenotype on the left, a short-tail (brachyury) phenotype in the middle, and a long-tail phenotype on the right (photo: Michaël Comte).

In Pembroke Welsh Corgis, the length of the natural bobtail varies from a complete tailless to a short tail with half the length of a normal tail and occasional kinks. For comparison, another likely recessively inherited type of bobtail exists in Bulldogs where all dogs in the breed have short tails with multiple kinks (Whitney 1947). There are also occasional reports of short-tailed dogs born from long-tailed parents in some breeds, revealing multiple patterns of inheritance or variations in penetrance.

We studied here the presence of the T gene mutation in a large number of breeds to investigate its possible ancestral origin and to identify whether other genetic causes exist in association with short tails. We tested 23 different breeds and showed that the C189G mutation is present in all short-tailed dogs of 17 breeds, supporting a correlation of mutation with the phenotype. We also showed that breeding of 2 bobtailed Swedish Vallhund dogs with the T gene mutation decreases litter size, which confirms a major role of T gene during embryogenesis.

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Materials and Methods

Animals and Definition of the Tail Phenotype

Samples were collected from 23 breeds including 360 dogs (156 short-tailed and 204 long-tailed dogs; Table 1). In addition, samples were collected from 80 dogs including 9 breeds presenting only the long-tail phenotype (American Cocker Spaniel, Bichon Frisé, English Setter, English Springer Spaniel, Golden Retriever, Long Haired Dachshund, Shih-Tzu, Smooth Dachshund, and Yorkshire Terriers). Pedigrees and tail phenotype information (anury, brachyury, and long tail) were collected from sampled dogs. Anury corresponds to a complete lack of vertebrae and brachyury to a short tail with variable lengths. Tail phenotypes were recorded by the sample collector, taken from the breeding database (Finnish Kennel Club 2008) or directly reported by the owners.

View this table:

Table 1

Genotyping results of the T gene mutation (C189G) for 23 different breeds harboring the short-tail phenotype

 Total No of dogs long-tail dogs Genotype C189 short-tail dogs  C189 
17 breeds with C189G mutation      
Australian Shepherd   70 42 C/C 28 C/G 
 Austrian Pinscher  C/C C/G 
Australian Stumpy Tail  Cattle Dog  C/G 
  Bourbonnais Pointer 25 16 C/C C/G 
Brazilian Terrier  17 C/C 10 C/G 
Brittany Spaniel   18 C/C 14 C/G 
Croatian Sheepdog   C/C C/G 
Danish/Swedish Farmdog C/C C/G 
Jack Russell Terrier  10 C/C C/G 
Karelian Bear Dog   C/C C/G 
Mudi  10 C/C C/G 
Polish Lowland  Sheepdog 28 10 C/C 18 C/G 
Pyrenean Shepherd  64 57 C/C C/G 
Savoy Sheepdog  17 15 C/C C/G 
Schipperke  12 C/C C/G 
Spanish Waterdog  C/C C/G 
Swedish Vallhund  22 C/C 16 C/G 
      
6 breeds without C189G mutation      
Boston Terrier  C/C C/C 
English Bulldog  C/C C/C 
King Charles Spaniel  22 13 C/C C/C 
Miniature Schnauzer  C/C C/C 
Parson Russell Terrier C/C C/C 
Rottweiler     

Genomic DNA Extraction

Samples were either ethylenediaminetetraacetic acid-blood or buccal cell samples. Genomic DNA was extracted from blood and buccal cells using either the NucleoSpin Kit (Macherey-Nagel, Hoerdt, France) or the BuccalAmp DNA Extraction Kit (Epicentre Biotechnologies, Madison, WI). Some samples with low DNA yields were amplified using the V2 Genomiphi Kit (GE Healthcare, Buckinghamshire, UK).

Polymerase Chain Reaction and Sequencing

The C189G mutation in exon 1 of the T gene was tested by polymerase chain reaction (PCR) from genomic DNA as previously described byHaworth et al. (2001) or with the following primer pair: 5′-AGAGCCTGCAGTACCGAGTG-3′ designed in exon 1 of the T gene and 5′-CCGAGACTTCTCCCAGAAAA-3′ designed in intron 1. The presence of the mutation in the amplified PCR product was detected by 1) restriction enzyme assay or 2) sequencing. 1) Restriction enzyme assay was performed with BstEII enzyme (New England Biolabs, Ipswich, MA) followed by visualization on agarose gel. All coding exons and surrounding splicing sites were sequenced for short-tailed dogs that did not have the mutation using primers and conditions as previously described by Haworth et al. (2001), except exon 8 in which we used the following primer pair: 5′-GCGGAGAAGGTGCCTTAGTA-3′ and 5′-CCTGGGAGGTCAATCAAATC-3′. 2) PCR products were cleaned by ExoSAP-IT (GE Healthcare) and sequenced with the BigDye Terminator v3.0 Cycle Sequencing Kit (Applied Biosystems, Foster City, CA) with ABI PRISM 3130XL DNA analyzer (Applied Biosystems). The resulting sequencing data were analyzed with the DNA Sequencing Analysis v5.2 software (Applied Biosystems). The nucleotide numbers indicated throughout this study have been defined from the Tgene translation initiation codon (GenBank AJ245513).

Statistical Analysis

The possible effect of the homozygous T gene mutation for embryonic viability was estimated by following the litter sizes of short-tailed parents compared with long-tailed parents in Swedish Vallhund breed. Statistical significance of the variation between the study groups was measured by Student’s t-test.

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Results

We analyzed the presence of the known T-box transcription factor T gene mutation, C189G (Ile63Met), in 23 breeds by genotyping 360 dogs including 156 short-tailed and 204 long-tailed dogs. We identified 17 breeds in which the short-tailed dogs carried the mutation and 6 breeds that did not (Table 1). Moreover, this mutation was not found in any dog from a set of 80 dogs belonging to 9 breeds that do not display naturally the short-tail phenotype (American Cocker Spaniel, Bichon Frisé, English Setter, English Springer Spaniel, Golden Retriever, Long Haired Dachshund, Shih-Tzu, Smooth Dachshund, and Yorkshire Terriers). These breeds increase the list of breeds analyzed by Haworth et al. (2001) from 19 to 28, thus confirming that this variant is not a nucleotide polymorphism. In the 6 breeds without the T gene mutation, in order to find any other variations in the T gene that could underlie the short-tail phenotype, we sequenced all the coding exons, exon/intron boundaries, and untranslated regions (UTR). The sequencing did not reveal any causative mutations in any of the 6 breeds. In addition to the several polymorphic sites described by Haworth et al. (2001), one novel nucleotide change present at the 5′ UTR (G-6A) was found in Miniature Schnauzers. However, this change did not segregate with the phenotype, indicating that it was a noncausative polymorphic site. This fact tends to exclude the entire T locus as causal for the phenotype in this Miniature Schnauzer pedigree, in which the short-tailed dogs are descendants of long-tailed parents. These results demonstrate that the T gene mutation is present in many but not all short-tailed dogs and that also other genetic factors are likely to regulate tail length.

Among the 315 dogs belonging to the 17 breeds identified here, all the 133 short tailed were heterozygous for the C189G T gene mutation and all the 182 long-tailed dogs did not carry the mutation. This result indicates the full penetrance and the lethality of the homozygous mutation. To further investigate the homozygous lethality, we calculated litter sizes for 2 parent combinations (long tailed × long tailed and short tailed × short tailed) for Swedish Vallhunds using the KoiraNet Breeding Database from the Finnish Kennel Club (2008) (Figure 2). Altogether, 253 puppies from 56 litters born between years 2000 and 2007 were included in the calculation. The average litter sizes were 5.5 puppies for long × long and 3.9 puppies for short × short crosses. The litter size reduction was 29% (P= 0.0008) for short × short crosses as compared with the long × long crosses. The observed 29% decrease, suggestive of an in utero lethality, is compatible with the expected 25% reduction in the litter size for short × short crosses because one-fourth of the puppies will inherit the mutation from both parents.

View larger version:

Figure 2

Comparison of litter sizes from different crosses in Swedish Vallhund breed. The average litter size is 5.5 puppies/litter with long-tail × long-tail crosses and 3.9 puppies/litter with short-tail × short-tail crosses. The litter size is reduced of 29% with short-tail × short-tail crosses (***P < 0.001) compared with the average litter size of long-tail × long-tail crosses. Results are expressed as mean (column value) ± standard error of the mean (bars on the top of the column).

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Discussion

Natural bobtailed dogs are present in many breeds but the causative mutation has been identified only for the Pembroke Welsh Corgis (Haworth et al. 2001), in which a dominantly inherited C189G mutation of the T-box transcription factor T gene (Ile63Met) results in a short-tail phenotype. In this study, we identified 17 additional breeds with this mutation, suggesting an ancestral origin of the T gene mutation. Indeed, these 17 breeds mainly belong to 2 groups: sheepdog and hunting breeds. All analyzed short-tailed dogs were heterozygous for the C189G mutation as previously shown for Corgis (Haworth et al. 2001). For the Swedish Vallhunds, analysis of the litter sizes from short-tailed × short-tailed crosses revealed a 29% reduction in litter size, further supporting recessive embryonic lethality of the mutation. In the Brittany Spaniel and Bourbonnais Pointer short-tailed × short-tailed crosses, such a reduction was not reported by the breeders; however, this observation being based on only few crosses, the reduction percentage could not be significantly calculated. Homozygosity for the mutation appears to cause either embryonic or early postnatal lethality due to serious developmental defects (Indrebø et al. 2007). Similar observations have been previously seen in different mouse mutants for the T gene (Gluecksohn-Schoenheimer 1938Wilson et al. 1995). Recently, Pembroke Welsh Corgi puppies with severe anatomical defects having the homozygous mutation have been characterized. These puppies lacked tails, manifested anorectal atresia with severe alterations in the posterior lumbar region and spine, and had a failure to thrive (Indrebø et al. 2007). In contrast with homozygous, heterozygous bobtailed dogs have not been reported to manifest any other abnormalities (Indrebø et al. 2007). In mouse mutants, additional spinal defects have been described in heterozygous T gene mutants. These phenotypic differences are most likely due to the different type of mutations in dogs and mice. Whereas the mutation in dogs affects only the T-box domain, mice carry large deletions that cover the whole Tgene and may also affect the other genes in the region such as the T2gene (Herrmann et al. 1990Rennebeck et al. 1998).

Although the T gene mutation is present in many breeds, it does not explain all short tail phenotypes. Boston Terrier, English Bulldog, King Charles Spaniel, Miniature Schnauzer, Parson Russell Terrier, and Rottweiler breeds all have natural short-tailed dogs but the analyzed bobtails carried neither the known C189G T gene mutation nor the other novel causative mutations within the same gene. The short-tail phenotype includes either a complete lack of vertebrae or a short tail with variable length. The T gene mutation can cause both anury and brachyury as illustrated in Figure 1. The 6 breeds above have both anury and brachyury, but the length and the number of kinks in these breeds are highly variable and could indicate heterogeneous genetic backgrounds. In mouse, mutations in genes such as Pax1Wnt-3aDII3, and Noto have been associated with short and kinked tails and, thus, remain as potential candidates (Gruneberg 1961Greco et al. 1996Wilm et al. 1998;Abdelkhalek et al. 2004Dunty et al. 2008). Short tail with multiple prominent kinks is a very common phenotype in King Charles Spaniel. Further analyses are underway to determine the mode of inheritance and the cause of the short-tailed phenotype in the breed. The rare short-tailed Miniature Schnauzers, Parson Russell Terrier, and Rottweilers that were part of the study were all born from long-tailed parents, suggesting a recessive model, spontaneous developmental abnormality (congenital and not hereditary), or a sporadic mutation. We are currently extending sample and pedigree collections in these breeds to address these questions. Boston Terriers and English Bulldogs all either lack or have very short and kinky tails, indicating that the phenotype is fixed and has become part of the breed characteristics. The mode of inheritance has been suggested to be recessive (Whitney 1947).

Tail docking is prohibited in many European countries, and the docked dogs cannot participate in official dog shows or trials unlike natural bobtails. The owner of the bobtailed dog needs a certificate from a veterinarian to prove the natural short tail to get access to shows. In the breeds harboring the mutation, veterinary inspections can now be replaced by the simple genetic test that confirms natural bobtails. Our study extends significantly the list of breeds that could benefit from the genetic testing.

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Funding

Ministère de la recherche et de l’enseignement supérieur to A.G.; Centre National de la Recherche Scientifique to B.H., S.D., S.S., F.G., and C.A.; the Academy of Finland to M.H., K.S. (project no. 214448), and H.L. (project no. 118463).

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Acknowledgments

We thank all participating breeders, veterinarians, and dog owners for the samples, especially Päivi Eerola, Michaël and Michel Comte; Pierre Willems, Christian Dagorne, Anka Obrist, Norbert Gainche, and the society “Amis des Epagneuls Nains Anglais”; and Dr B. Denis and Dr B. Cattanach BSc, PhD DSc, FRS, for helpful discussions.

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Footnotes

  • * These authors equally contributed to the work
  •  These laboratories equally contributed to the work
  • Corresponding Editor: Elaine Ostrander
  • © The American Genetic Association. 2008. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org.

Tail docking is not a new phenomenon; neither is opposition to it. In 1896, the Kennel Club in England debated a motion that would ban any docked dog from winning a prize at a dog show. Tail docking is prohibited in many countries. In Europe, some breeders are turning to dogs with natural bobtails in an attempt to keep that short-tail look without docking.

Will bobs catch on for all breeds?

Maybe. Several traditionally docked breeds also have individuals with natural bobtails. Early Pembroke Welsh Corgis, for example, had tails that were more short than long, the short ones ranging from short bobs to half-length terrier-type tails. The early Corgi standard requested “tail short.”

http://www.dogster.com/wp-content/uploads/2015/05/male-pug-profile.gifPugs’ tails are naturally short and curly.

But what of breeds in which no natural bobs exist? Boxers, for example. In 1992, Dr. Bruce Cattanach, geneticist and longtime Boxer breeder, introduced Corgi bobtail genes into his Boxer line. He bred his Boxer female to a Corgi male with a natural bobtail, then crossed the bobtailed progeny back to Boxers for several generations. By the fourth generation he had Boxers that looked indistinguishable from other Boxers, except that some (not all) had natural bobtails.

But he still couldn’t get his line to consistently produce bobs. Some breeds, such as Bulldogs and Boston Terriers, do in fact breed true for naturally short tails. Why not Corgis and Boxers? It took a DNA study to find the answer.

The bobtail mutation is a dominant trait

It turns out a different mutation causes the short tails in Bulldogs and Bostons versus Corgis and Australian Shepherds, for example. The mutation in Corgis is called a T-box mutation. of the 23 breeds in which natural bobs were found, 17 had bobs caused by this T-box mutation. These included the Australian Shepherd, Brittany,Karelian Bear DogPolish Lowland SheepdogPyrenean ShepherdSchipperkeSwedish Vallhund and Russell Terrier. In each of the dogs of these breeds with natural bob tails, one (and only one) copy of the T-box gene was found.

These findings indicate that the bobtail mutation acts as a dominant trait, and suggest that having two copies of the mutation is lethal. In fact, the T-box mutation in mice is known to cause embryonic death. Turns out the same is true for dogs.

http://www.dogster.com/wp-content/uploads/2015/05/boxer-bob-tail-chasing-dog.gifBoxers don’t generally have natural bobs.

In looking at 56 litters of Swedish Valhunds of either long-to-long-tail matings or bobtail-to-bobtail matings, researchers found that litter size was reduced by 29 percent in the bob-to-bob litters — exactly what you would predict if one quarter of embryos were homozygous bobs and died in utero. This means you can never have a true breeding line of natural bob-tailed dogs — or at least, ones caused by the T-box mutation.

But remember, not all bobtails are caused by the T-box mutation. The Bulldog and Boston Terrier both breed true for short tails. Their tails, which are also usually screwed or kinked, are caused by a recessive gene that has not yet been identified.

http://www.dogster.com/wp-content/uploads/2015/05/boston-terrier-butt.jpgWhat’s up, Boston butt? Photo by Pam Mitchell.

The controversy of docking tails is bound to heat up. Those opposed to tail docking cite pain felt by puppies, mutilation of dogs’ bodies, deprivation of dogs’ communicative and balancing apparatus, and the possibility of medical complications as reasons to cease the practice. Proponents of docking counter that tail docking is needed to maintain breed type, maintain hygiene, and prevent injury in working and hunting dogs.

Could the introduction of natural bobtails be the compromise that would make both sides happy? Probably not entirely. Because of the situation with lethal homozygotes, breeders will have to settle either for about a quarter of puppies dying before birth, or for always having long tails along with bobs. And not everyone could flock to the few natural bobs around — that would be bad for the gene pool and cause other problems. But natural bobs do offer an alternative for some breeders, and certainly breeders who have them should appreciate their potential value.

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