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Boston Terrier

Lifespan
11.8 years
95% CI 11 to 12.2 · McMillan 2024, n=1,984
Most carried variant
Degenerative Myelopathy
7.7% of 3,702 tested · Donner 2023
Behind this page
31 dogs
in the atlas · an early sketch · 3,702 tested for variants
Also carried:Canine Multifocal Retinopathy 1 · 7.5%Cystinuria Type I-A · 3%

Boston Terriers have a cited life expectancy of 11.8 years (McMillan 2024 / VetCompass, n=1,984, 95% CI 11 to 12.2). The most carried tested variant is Degenerative Myelopathy, in 7.7% of 3,702 Boston Terriers tested (Donner 2023), then Canine Multifocal Retinopathy 1 (7.5%) and Cystinuria Type I-A (3%). 31 dogs stand behind the atlas figures here, so treat this page as an early sketch.

Boston Terrier
Photo: Andreas Schlaugat · CC BY 3.0 · Wikimedia

Also known as American Gentlemen, Boston Bull, Boston Bull Terrier, and Boxwood.

See in the atlas → From CanVAS
Mendelian-disease genetics

What genetic diseases do Boston Terriers carry?

From a panel of 250 Mendelian-disease variants screened in 1,054,293 dogs (Donner et al. 2023), Boston Terriers carry 20 of them at observable frequency. Carrier frequency is not clinical risk. Most recessive variants require two copies for disease expression; many dominant variants show incomplete penetrance. Read this as a population fingerprint of what's in the gene pool, not a per-dog prediction.

Chondrodystrophy and Intervertebral Disc Disease Risk (CDDY)
Autosomal dominant
moderate 2.0%
n = 3,685 dogs · 1 variant tested · OMIA:000157-9615 · omia.org →
FGF4what this gene does

FGF4 influences leg length by affecting bone growth, leading to shorter legs in certain breeds.

For your dog: If your dog is from a breed known to carry this gene, it's worth discussing spinal health with your vet, but being a carrier doesn’t guarantee problems.

Degenerative Myelopathy (DM)
Autosomal recessive (Incomplete penetrance)
low 7.7%
n = 3,702 dogs · 1 variant tested · OMIA:000263-9615 · omia.org →
SOD1what this gene does

SOD1 is a gene that helps protect cells from damage caused by harmful molecules called free radicals.

For your dog: If your dog is a carrier of SOD1 variants, it's worth discussing with your vet, but remember carrier status doesn't mean your dog will get the disease.

Canine Multifocal Retinopathy 1 (Discovered in Mastiff-related breeds; CMR1)
Autosomal recessive
low 7.5%
n = 3,702 dogs · 1 variant tested · OMIA:001444-9615 · omia.org →
BEST1what this gene does

BEST1 is a gene that helps maintain the health of the retina, the light-sensitive layer at the back of the eye. It plays a role in keeping the cells in the retina functioning properly.

For your dog: If your dog is from a breed known to carry BEST1 variants, it’s worth discussing retinal health with your vet, especially if you notice any vision changes.

Cystinuria Type I-A (SLC3A1 p.I192V)
Autosomal recessive
low 3.0%
n = 3,702 dogs · 3 variants tested · OMIA:000256-9615 · omia.org →
SLC3A1what this gene does

SLC3A1 is a gene that helps transport certain amino acids in the kidneys. It plays a key role in preventing the buildup of cystine, which can form stones.

For your dog: If your dog is from a breed known to carry SLC3A1 variants, it’s worth discussing cystinuria risks with your vet, especially if urinary issues arise.

Dilated Cardiomyopathy risk factor (Discovered in the Doberman Pinscher; PDK4-related)
Autosomal dominant (Incomplete penetrance)
marker disputed 2.8%
n = 3,702 dogs · 2 variants tested · OMIA:000162-9615 · omia.org →
PDK4what this gene does

PDK4 helps regulate how cells use energy, especially in the heart muscle.

For your dog: If your dog is one of the breeds known to carry this gene, it’s worth discussing heart health with your vet, but being a carrier doesn’t mean your dog will develop disease.

Craniomandibular Osteopathy (Discovered in the Cairn, Scottish and West Highland White Terrier)
Autosomal dominant (Incomplete penetrance)
low 0.92%
n = 3,702 dogs · 1 variant tested · OMIA:002244-9615 · omia.org →
SLC37A2what this gene does

SLC37A2 is a gene involved in how cells manage certain sugar molecules, which can affect bone development.

For your dog: If your dog is from a breed known to carry this gene variant, it's worth discussing with your vet, especially if you notice jaw discomfort or eating issues.

Hyperuricosuria (HUU)
Autosomal recessive
low 0.81%
n = 3,702 dogs · 1 variant tested · OMIA:001033-9615 · omia.org →
SLC2A9what this gene does

SLC2A9 is a gene that helps regulate uric acid levels in a dog's body. It plays a role in how the kidneys handle this substance.

For your dog: If your dog is one of the breeds known to carry this gene variant, it’s worth discussing with your vet to understand any potential urinary health concerns.

Cone-Rod Dystrophy (cord1-PRA/crd4)
Autosomal recessive (Incomplete penetrance)
low 0.68%
n = 3,696 dogs · 1 variant tested · OMIA:001432-9615 · omia.org →
RPGRIP1what this gene does

RPGRIP1 is a gene involved in the function of photoreceptor cells in the eye, which help dogs see in different light conditions.

For your dog: If your dog belongs to a breed known to carry RPGRIP1 mutations, it’s worth discussing with your vet to understand the risks and monitor eye health.

Cystinuria Type I-B (SLC7A9 p.A217T)
Autosomal recessive (Incomplete penetrance)
marker disputed 0.49%
n = 3,702 dogs · 2 variants tested · OMIA:001880-9615 · omia.org →
SLC7A9what this gene does

SLC7A9 is a gene that helps transport certain amino acids in the kidneys. It plays a role in how the body handles cystine, an amino acid that can form crystals.

For your dog: If your dog is a carrier, it’s worth discussing with your vet to monitor urinary health and catch any issues early.

Von Willebrand's Disease, Type 1 (vWD 1)
Autosomal recessive
low 0.26%
n = 3,702 dogs · 1 variant tested · OMIA:001057-9615 · omia.org →
Bleeding disorder (Discovered in the Greater Swiss Mountain Dog; P2RY12-related)
Autosomal recessive
low <0.1%
n = 3,701 dogs · 1 variant tested · OMIA:001564-9615 · omia.org →
P2RY12what this gene does

P2RY12 is a gene that helps control how platelets stick together to form blood clots, which is essential for stopping bleeding.

For your dog: If your dog is from one of these breeds, it’s worth asking your vet about P2RY12 to understand any potential bleeding risks, especially before surgery or injury.

Progressive Rod-Cone Degeneration (prcd-PRA)
Autosomal recessive
low <0.1%
n = 3,699 dogs · 1 variant tested · OMIA:001298-9615 · omia.org →
PRCDwhat this gene does

PRCD is a gene involved in the health of a dog's retina, the part of the eye that detects light and helps with vision.

For your dog: If your dog belongs to a breed known to carry PRCD changes, it's worth discussing eye health and potential genetic testing with your vet.

Limb-girdle Muscular Dystrophy, Type 2F (Discovered in the Boston Terrier)
Autosomal recessive
low <0.1%
n = 3,702 dogs · 1 variant tested · OMIA:002122-9615 · omia.org →
Musladin-Lueke syndrome (MLS)
Autosomal recessive
Likely pathogenic / pathogenic low <0.1%
n = 3,701 dogs · 1 variant tested · OMIA:001509-9615 · omia.org →
ADAMTSL2what this gene does

ADAMTSL2 is a gene that helps regulate the structure and function of connective tissues in the body.

For your dog: If your dog is from a breed known to carry this gene variant, it's worth discussing with your vet, especially if you notice unusual stiffness or facial traits.

Amelogenesis Imperfecta (Discovered in the Parson Russell Terrier; AI)
Autosomal recessive
low <0.1%
n = 3,702 dogs · 2 variants tested · OMIA:001805-9615 · omia.org →
ENAMwhat this gene does

ENAM is a gene that helps form enamel, the hard outer layer of teeth. It plays a key role in making sure teeth develop strong and smooth.

For your dog: If your dog is from one of these breeds, it’s worth asking your vet about ENAM and dental health, especially if you notice unusual wear or discoloration on their teeth.

Neuronal Ceroid Lipofuscinosis 4A (Discovered in the American Staffordshire Terrier; NCL4A)
Autosomal recessive
Pathogenic low <0.1%
n = 3,702 dogs · 1 variant tested · OMIA:001503-9615 · omia.org →
ARSGwhat this gene does

ARSG is a gene that helps break down certain molecules in the body, keeping cells healthy.

For your dog: If your dog is from a breed known to carry ARSG mutations, it's worth discussing genetic testing with your vet to understand potential health risks.

Acral Mutilation Syndrome (AMS)
Autosomal recessive
low <0.1%
n = 3,702 dogs · 1 variant tested · OMIA:001514-9615 · omia.org →
GDNFwhat this gene does

GDNF is a gene that helps support nerve cells, especially those involved in sensing pain and movement.

For your dog: If your dog is from a breed that can carry this gene change, it’s worth asking your vet about testing to understand any potential risks.

Chondrodysplasia, Disproportionate Short-limbed (Discovered in the Norwegian Elkhound; ITGA10-related)
Autosomal recessive
low <0.1%
n = 3,702 dogs · 1 variant tested · OMIA:001886-9615 · omia.org →
Collie Eye Anomaly (CEA)
Autosomal recessive
low <0.1%
n = 3,702 dogs · 1 variant tested · OMIA:000218-9615 · omia.org →
NHEJ1what this gene does

NHEJ1 is a gene involved in repairing breaks in DNA, helping maintain the integrity of genetic information in cells.

For your dog: If your dog belongs to one of the breeds known to carry this gene variant, it's worth discussing testing with your vet to understand any potential eye health risks.

Congenital Myasthenic Syndrome (Discovered in the Heideterrier; CHRNE-related; CMS)
Autosomal recessive
low <0.1%
n = 3,702 dogs · 2 variants tested · OMIA:000685-9615 · omia.org →
CHRNEwhat this gene does

CHRNE is a gene involved in the communication between nerves and muscles, helping muscles respond properly to signals.

For your dog: If your dog is from a breed known to carry CHRNE variants, it's worth discussing with your vet, especially if you notice muscle weakness or unusual fatigue.

Source: Donner J et al. 2023. Genetic prevalence and clinical relevance of canine Mendelian disease variants in over one million dogs. PLOS Genetics 19(2):e1010651 · Evidence: Limited (DTC ascertainment, tag-SNP proxy) · Confounding MEDIUM · License CC-BY-4.0 · Phene IDs from OMIA (Sydney School of Veterinary Science, The University of Sydney; DOI 10.25910/2AMR-PV70).
Sample size in this breed: 3,702 dogs from the Donner 2023 cohort.
In plain terms

What these results mean for a Boston Terrier

Chondrodystrophy and disc disease risk (CDDY)

2.0% of Boston Terriers in the Donner 2023 cohort carried it (n=3,685).

  • Two extra copies of a growth gene, FGF4, shape dog legs and spines. The one on chromosome 12 is the one tied to disc disease; the one on chromosome 18 shortens legs.
    OMIA 000157-9615

    “Two FGF4 retrogenes (FGF4L1 on chromosome 18 and FGF4L2 on chromosome 12) have been identified to cause dwarfism across many dog breeds.” OMIA 000157-9615

    “Brown et al. (2017) reported that an FGF4 retrogene insertion in chromosome CFA12” OMIA 000157-9615

  • Carrying it raises risk. It does not say which dog will have a disc problem. In Dachshunds researchers found the test is not a valid risk indicator on its own.
    OMIA 000157-9615

    “the FGF4 retrogene insertion on CFA12 is not a valid risk indicator on its own” OMIA 000157-9615

What to do
Ask your veterinarian what a carrier result changes for your dog. What lowers risk in a carrier is not established in the sources this page draws on.

No test, or a mix
Without a test nobody can say whether a dog carries it. Leg length alone does not tell you: the disc-disease copy and the short-leg copy are different insertions.

Degenerative myelopathy (DM)

7.7% of Boston Terriers in the Donner 2023 cohort carried it (n=3,702).

  • DM is a loss of function in the spinal cord that begins in adulthood and progresses to paralysis of the back legs. There is no treatment that stops it.
    OMIA 000263-9615

    “This is an adult onset degeneration of the spinal cord that progresses to paraplegia and tetraparesis. There is no successful treatment. A genetic test is available.” OMIA 000263-9615

  • Two copies of the SOD1 variant mean at risk, not affected. Some dogs with two copies never show signs.
    OMIA 000263-9615

    “some homozygous mutant dogs had no signs of degenerative myelopathy, which suggests incomplete penetrance or other causative loci” OMIA 000263-9615

  • One copy makes a dog a carrier. In the study that found the variant, every affected dog tested had two copies.
    OMIA 000263-9615

    “All affected dogs tested were homozygous mutant.” OMIA 000263-9615

What to do
A DNA result is not a diagnosis. Take the result, and any change in how the dog walks, to a veterinarian.

No test, or a mix
Without a test nobody can say how many copies a dog has. A breed's carrier frequency describes the breed, not this dog.

Cystinuria type I-A (SLC3A1)

3.0% of Boston Terriers in the Donner 2023 cohort carried it (n=3,702).

  • The kidneys fail to reclaim an amino acid called cystine, which can form crystals and stones in the urine and block the urinary tract.
    OMIA 000256-9615

    “Cystinuria, type 1 - A is an inherited defect that causes failure of reabsorption of cystine in the proximal renal tubule, leading to cystine precipitation in the urine. Formation of crystals and calculi lead to urolithiasis and urinary tract obstruction.” OMIA 000256-9615

What to do
Straining to urinate, or passing little or no urine, needs a veterinarian the same day.

No test, or a mix
Without a test nobody can say how many copies a dog has.

Dilated cardiomyopathy marker (PDK4-related, first reported in Dobermans)

Marker disputed

2.8% of Boston Terriers in the Donner 2023 cohort carried it (n=3,702).

  • This is a marker, not an established cause. The curated record says a test based on it is not a good indicator of heart disease risk even in Dobermans, the breed it was found in.
    OMIA 000162-9615

    “it is evident that any DNA test based on this marker will not be a good indicator of liability to this disorder in Dobermans” OMIA 000162-9615

What to do
A carrier result for this marker is not, on its own, a reason for heart screening. Heart screening is a conversation with your veterinarian about the breed and the dog.

No test, or a mix
What this marker means in breeds other than the Doberman is not established in the sources this page draws on.

Which Mendelian variants matter most for Boston Terriers?

The Mendelian-disease table above lists variants screened in 3,702 Boston Terriers (Donner 2023). Four variants define the breed’s genetic-disease landscape, with two carrying substantially higher risk.

Canine Multifocal Retinopathy 1 (CMR1)

Canine Multifocal Retinopathy 1 is an autosomal-recessive eye condition discovered in Mastiff-related breeds and now identified in Boston Terriers. In Boston Terriers the figure below is a carrier frequency from Donner 2023, not a case series in the breed. The variant causes multiple areas of retinal dysfunction. 7.5% of Boston Terriers carry one copy (n=3,702). Importantly, Donner 2023 found zero of one at-risk homozygous dog phenotype-confirmed, which is too few to state a penetrance figure and leaves clinical expression in Boston Terriers unconfirmed despite the variant’s presence.

Testing is available. The low confirmed penetrance in this breed suggests the condition may be less clinically significant in Boston Terriers than in other breeds, but affected dogs warrant ophthalmologic screening.

What should I feed a Boston Terrier?

Feeding a Boston Terrier well means feeding around the breed’s known genetic vulnerabilities and its brachycephalic anatomy. Boston Terriers cannot pant efficiently, which means heat-of-the-day exercise is dangerous and meal timing matters more than it does for most breeds.

Grain-free, pulse-heavy diets carry cardiac risk for this breed. The FDA’s 2018 advisory flagged an association between grain-free, legume-heavy diets and dilated cardiomyopathy across multiple breeds (FDA 2018 DCM advisory). Boston Terriers meet both criteria. The conservative default is a grain-inclusive, taurine-supplemented adult formulation from a manufacturer that runs feeding trials. Taurine adequacy should be confirmed with your veterinarian or a board-certified veterinary nutritionist.

Meal timing and ambient temperature are non-negotiable. Boston Terriers should eat their largest meal in cooler parts of the day (early morning or evening), never in heat. Smaller, more frequent meals reduce the risk of gastric dilatation and also help stabilize energy throughout the day.

Joint support and weight management prevent disc-disease escalation. Disc disease is reported in the breed, though only 2.0% of Boston Terriers carry the CDDY insertion (Donner 2023, n=3,685). Adult-life weight should stay at the lean end of the breed standard. Weight management and controlled activity are the most evidence-based approaches for dogs with early disc-disease signs. Starting joint-support supplements in middle-aged Boston Terriers with any spinal-pain history is a common clinical practice, though individual benefit varies. Omega-3 fatty acid supplementation (EPA and DHA) is commonly recommended for joint support; consult your veterinarian for appropriate dosing.

Sodium and cardiac health. If a Boston Terrier has developed a cardiac murmur or been diagnosed with dilated cardiomyopathy, sodium restriction becomes important. The appropriate sodium threshold varies by cardiac stage and should be guided by your veterinary cardiologist. Do not restrict sodium without cardiac diagnosis; healthy dogs need adequate sodium for osmotic balance.

What we don’t know

Craniomandibular osteopathy penetrance in Boston Terriers appears low (1 of 11 at-risk dogs phenotype-confirmed, Donner 2023), too few to state a figure. The variant is present at 0.92% carrier frequency (n=3,702), but clinical expression in the breed appears rare. We do not yet have a clear explanation for why this variant, common in Scottish and West Highland White Terriers, causes so little disease in Boston Terriers.

The Atlas contains only 31 Boston Terriers, which is a small cohort. Longevity patterns and rare-disease epidemiology may shift as more Boston Terriers enter the database. Longevity patterns, rare-disease epidemiology, and founder-bottleneck effects may shift as more Boston Terriers enter the database. The breed’s genetic diversity rank of 80 of 107 suggests tighter founder structure than average; additional data will clarify whether this has contributed to disease frequency.

Frequently asked questions about Boston Terriers

What is the most common genetic issue in Boston Terriers? Degenerative myelopathy carries the highest frequency at 7.7% carrier rate (Donner 2023, n=3,702). A carrier with one copy is not itself at risk; the disease shows up in dogs with two copies, and even then how often it actually develops is genuinely debated, so a result here is a marker to track in breeding, not a verdict on a dog. Canine Multifocal Retinopathy 1 is also at 7.5% carrier frequency and is generally a mild, non-progressive finding in the breed.

Do Boston Terriers get back problems? About 2.0% of Boston Terriers carry the CDDY insertion that raises intervertebral disc disease risk (Donner 2023, n=3,685). For any Boston Terrier, weight management, avoiding jumping from heights, and early treatment of any spinal pain reduce severity.

How long do Boston Terriers live? Cited life expectancy is 11.8 years (McMillan 2024 / VetCompass, n=1,984, 95% CI 11 to 12.2). Individual lifespan varies with cardiac and neurological health, weight management, and access to preventive screening.

Can I do a DNA test to know if my Boston Terrier will get degenerative myelopathy? Testing identifies carrier status and homozygous-affected dogs. Carriers have a risk of producing affected offspring if bred to another carrier. Homozygous-affected dogs have the genetic predisposition but may never show symptoms due to incomplete penetrance; screening for early neurological signs is prudent.

What is the best diet for a Boston Terrier? Grain-inclusive, taurine-supplemented formulations are safest given the breed’s cardiac vulnerability and brachycephalic anatomy. Feed larger meals in cool parts of the day, avoid grain-free diets, and keep weight at the lean end of the breed standard to support joint health.

Are Boston Terriers good with children? Boston Terriers are companion dogs with historically stable temperament. Individual socialization and training matter more than breed predisposition. Their small size and brachycephalic anatomy mean they overheat easily, so play sessions should be brief and in cool conditions.

Do Boston Terriers shed a lot? Boston Terriers have short, smooth coats and shed moderately year-round, with heavier shedding during seasonal coat blows. Regular brushing reduces loose hair in the home.

Temperament

What Boston Terriers tend toward

Tendencies from owner surveys of purebred Boston Terriers — a leaning across the breed, not a prediction for any one dog. A bar’s strength shows how much of that behavior breed actually explains: for most it’s faint, because the rest is your dog, their training, and the life you give them.

Environmental Engagementbreed ~9%
high engagementlow engagement
Toy-directed Motor Patternsbreed ~18%
toy-directednot toy-directed
Human Sociabilitybreed ~11%
less sociablehighly sociable
Dog Sociabilitybreed ~8%
less sociablehighly sociable
Proximity Seekingbreed ~13%
affectionatealoof
Agonistic Thresholdbreed ~9%
assertivediffident
Biddabilitybreed ~18%
biddableindependent
n = 28 dogs · Morrill et al. 2022, Science, Darwin's Ark (CC0)
Owner-reported purebreds; each factor n ≥ 25. "Breed ~%" is the share of this behavior explained by breed.
Names & origins

Other names

The Boston Terrier is also recorded as American Gentlemen, Boston Bull, Boston Bull Terrier, and Boxwood.

Identified as Boston Terrier (VBO:0200204) in the Vertebrate Breed Ontology (Mullen et al. 2025, CC-BY 4.0) · registry IDs FCI 140 · iDog 46 · VeNom 14963.

For researchers Population genetics, disease models and every recorded condition Open the research detail for the Boston Terrier
What the atlas says about Boston Terrier

In the atlas, the Boston Terrier clusters consistently as Boston Terrier (100% of the 31 dogs here). Genetic diversity is high (mean heterozygosity 0.3347), reflecting either a mixed-breed cluster or breeds with broad genetic backgrounds. Dogs here sit in a relatively sparse region of the atlas, fewer close neighbors than typical.

Mean heterozygosity is 0.335, notably high, indicates broad genetic background.

Genetic dimensions · CanVAS atlas

What the atlas genotypes say about Boston Terrier

Computed from the 14,478 CanVAS dogs in the Atlas, on an imputed genotype backbone: 77,215 directly typed sites per dog, imputed to 9.67 million variants.

The confidence below counts dogs, not reads: it is the size of the sample, and it is separate from how the genotypes were measured.

Dogs in the Atlas
31Founders
21 from Hayward2016, 10 from Spatola
Genetic diversity
0.33Moderate
Mean heterozygosity across the breed. 28th most diverse of 107 ranked populations.
What does genetic diversity mean?

How varied a breed's gene pool is — the share of gene spots where a typical dog of the breed carries two different versions rather than two identical ones.

How to read it: Higher = more diverse. Among well-sampled breeds it ranges roughly 0.22 (least diverse) to 0.33 (most diverse).

Diversity is a strength, not a verdict on any individual dog. Lower diversity means it's worth paying attention to recessive-risk testing — not that a dog is doomed.

Cluster structure
Splits into two genetic sub-populations
Intra-breed RMS distance: 23.41 · likely working/show-line, regional, or kennel lineage split.
What does within-breed variation mean?

How much individual dogs within the breed differ from each other genetically.

How to read it: Higher = more internal variety among individuals of the breed.

Sensitive to how many dogs of the breed we've sampled.

Related breeds
Built from
Close cousins
Distant kin · one shared founding ancestor
In the Non-Sporting group
Explore the full lineage map →
VBO foundation stock (breeding records) · AKC breed group
Relatedness is documented lineage + kennel family. Genetic-ancestry distance measures diversity, not kinship, so it isn't used here.
How long they live
11.8years (life expectancy)
95% CI 11–12.2 · VetCompass, McMillan 2024, n=1,984. source
What does typical lifespan mean?

The median age dogs of the breed tend to reach.

How to read it: Higher = longer-lived. Compare to longevity-for-size to see whether it's just a size effect.

Drawn from population lifespan records; individual dogs vary widely with care, genetics, and luck.

n = 31 dogs · moderate sample · CanVAS (Brundage 2026) · Sniff Atlas
A gift to human medicine

Boston Terriers are a natural model for human disease

Because the same genes cause the same conditions across species, the inherited conditions documented in Boston Terriers help researchers understand, and work toward treating, the human diseases they model. This is the dog advancing human medicine. The breed models the human disease; it does not have it, and this is not a prediction for your dog.

Human equivalents via OMIA → Mondo / OMIM. Model-of, not identity. The named gene is the canine locus, not a claim that a pet has the human disease.
Documented in OMIA

Every condition recorded in the Boston Terrier

Beyond the testable carriers above, OMIA's literature catalogue records 6 genetic conditions in the Boston Terrier, 5 of which have a known human equivalent. This is the documented landscape across all Boston Terriers ever studied, not a prediction for any one dog.

Online Mendelian Inheritance in Animals (OMIA); Nicholas, Tammen & Sydney Informatics Hub, DOI 10.25910/2AMR-PV70
Documented in the breed's literature is not carrier status and not a forecast for an individual dog. Human equivalents are mapped via Mondo/OMIM. Carrier frequencies (above) are the separately-measured testable subset (Donner 2023).
The data behind this page

Where every number on this page came from.

This page draws on three primary data sources. Carrier frequencies for the Mendelian section come from Donner et al. 2023 (CC-BY-4.0). We grade these data at evidence Limited because the cohort is a direct-to-consumer ascertainment, which biases toward owners who chose to test their dogs. The panel also uses tag-SNP proxies for some variants rather than direct causal-variant assays. Limited is a study-design grade, not a quality grade: the Donner cohort is the largest open canine-genotype dataset in existence and we are grateful for it. We rate the confounding MEDIUM.

Population-genetic dimensions (heterozygosity, intra-breed PCA distance, nearest neighbors, trait-locus frequencies) come from CanVAS (Brundage 2026), harmonized through the Sniff Atlas. The exact release date and verification commit are pinned at the bottom of the page so a researcher can trace a number back to a specific snapshot. The disease-gene-variant graph comes from OMIA (Online Mendelian Inheritance in Animals; Nicholas, Tammen, and the Sydney Informatics Hub at the Sydney School of Veterinary Science, The University of Sydney; retrieved April 2026, DOI 10.25910/2AMR-PV70).

What this page does not yet have. Inheritance modes and per-disease penetrance evidence from Donner 2023 are in the structured data for every variant the panel covers. Mondo, OMIM, Ensembl, and HGNC cross-references live on the gene and disease pages this page links to, rather than being repeated here. What is still absent from this breed page is anything not in the cited panel, and each such gap carries its cause where it appears.

How to cite this page. The computed dimensions on this page are derived from the open Sniff Atlas v1.0.1 (Gehring 2026, doi:10.5281/zenodo.20566358, CC-BY 4.0). Full citation formats including BibTeX, RIS, and CITATION.cff at sniff.world/cite.

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References
  1. Donner J, Freyer J, Davison S, Anderson H, Blades M, Honkanen L, et al. (2023). Genetic prevalence and clinical relevance of canine Mendelian disease variants in over one million dogs. PLOS Genetics 19(2):e1010651. doi:10.1371/journal.pgen.1010651
  2. Brundage DM (2026). CanVAS: A Harmonized and Imputed Canine Variant Atlas. bioRxiv. doi:10.64898/2026.04.13.718238
  3. Nicholas, F.W., Tammen, I., & Sydney Informatics Hub. (2026). Online Mendelian Inheritance in Animals (OMIA) [dataset]. The University of Sydney. https://omia.org. doi:10.25910/2AMR-PV70 (retrieved April 2026).
Last updated
Sources: CanVAS (Brundage 2026) · Donner 2023 · OMIA