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Pug

Lifespan
11.6 years
95% CI 11.4 to 11.8 · McMillan 2024, n=10,026
Most carried variant
Degenerative Myelopathy
26% of 5,154 tested · Donner 2023
Behind this page
31 dogs
in the atlas · an early sketch · 5,154 tested for variants
Also carried:Von Willebrand's Disease, Type 1 · 2.1%Chondrodystrophy and Intervertebral Disc Disease Risk · 1.5%

Pugs have a cited life expectancy of 11.6 years (McMillan 2024 / VetCompass, n=10,026, 95% CI 11.4 to 11.8). The most carried tested variant is Degenerative Myelopathy, in 26% of 5,154 Pugs tested (Donner 2023), then Von Willebrand's Disease, Type 1 (2.1%) and Chondrodystrophy and Intervertebral Disc Disease Risk (1.5%). 31 dogs stand behind the atlas figures here, so treat this page as an early sketch.

Pug
Photo: Xidrep · CC BY-SA 3.0 · Wikimedia

Also known as Carlin, Chinese pug, Dutch bulldog, and Dutch mastiff.

See in the atlas → From CanVAS
Mendelian-disease genetics

What genetic diseases do Pugs carry?

From a panel of 250 Mendelian-disease variants screened in 1,054,293 dogs (Donner et al. 2023), Pugs carry 25 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.

Degenerative Myelopathy (DM)
Autosomal recessive (Incomplete penetrance)
high 26.0%
n = 5,154 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.

Chondrodystrophy and Intervertebral Disc Disease Risk (CDDY)
Autosomal dominant
moderate 1.5%
n = 5,136 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.

Von Willebrand's Disease, Type 1 (vWD 1)
Autosomal recessive
low 2.1%
n = 5,154 dogs · 1 variant tested · OMIA:001057-9615 · omia.org →
Cone-Rod Dystrophy (cord1-PRA/crd4)
Autosomal recessive (Incomplete penetrance)
low 0.27%
n = 5,145 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-A (SLC3A1 p.I192V)
Autosomal recessive
low 0.17%
n = 5,154 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.

Progressive Retinal Atrophy (Discovered in the Giant Schnauzer; NECAP1-related)
Autosomal recessive
low <0.1%
n = 5,154 dogs · 1 variant tested · OMIA:002198-9615 · omia.org →
Progressive Rod-Cone Degeneration (prcd-PRA)
Autosomal recessive
low <0.1%
n = 5,146 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.

Canine Multifocal Retinopathy 1 (Discovered in Mastiff-related breeds; CMR1)
Autosomal recessive
low <0.1%
n = 5,154 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.

Dilated Cardiomyopathy risk factor (Discovered in the Doberman Pinscher; PDK4-related)
Autosomal dominant (Incomplete penetrance)
marker disputed <0.1%
n = 5,154 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.

Cystinuria Type I-B (SLC7A9 p.A217T)
Autosomal recessive (Incomplete penetrance)
marker disputed <0.1%
n = 5,154 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.

Primary Lens Luxation (PLL)
Autosomal recessive
Pathogenic low <0.1%
n = 5,154 dogs · 2 variants tested · OMIA:000588-9615 · omia.org →
ADAMTS17what this gene does

ADAMTS17 is a gene that influences body size and also plays a role in certain eye conditions. It affects the structure of tissues in the eye and elsewhere in the body.

For your dog: If your dog belongs to a breed known to carry ADAMTS17 variants, it’s worth discussing genetic testing and eye exams with your vet to stay ahead of potential issues.

Full ADAMTS17 gene page →
Craniomandibular Osteopathy (Discovered in the Cairn, Scottish and West Highland White Terrier)
Autosomal dominant (Incomplete penetrance)
low <0.1%
n = 5,154 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.

Hypocatalasia
Autosomal recessive
low <0.1%
n = 5,154 dogs · 1 variant tested · OMIA:001138-9615 · omia.org →
CATwhat this gene does

CAT is a gene that helps produce an enzyme called catalase, which breaks down hydrogen peroxide in the body to prevent cell damage.

For your dog: If your dog is from a breed that can carry this gene, it’s worth asking your vet about testing. Being a carrier doesn’t mean your dog is affected, but it can inform health decisions.

Pituitary-Dependent Hyperadrenocorticism (Discovered in Poodles)
Autosomal dominant
low <0.1%
n = 5,154 dogs · 1 variant tested · OMIA:000247-9615 · omia.org →
Shar-Pei Autoinflammatory Disease (SPAID)
Autosomal dominant (Incomplete penetrance)
low <0.1%
n = 5,154 dogs · 1 variant tested · OMIA:001561-9615 · omia.org →
MTBPwhat this gene does

MTBP is a gene involved in regulating inflammation in the body. It helps control how the immune system responds to triggers.

For your dog: If your dog is from a breed known to carry MTBP variants, it's worth discussing with your vet whether genetic testing or monitoring for inflammation-related issues makes sense.

Factor VII Deficiency
Autosomal recessive
low <0.1%
n = 5,153 dogs · 1 variant tested · OMIA:000361-9615 · omia.org →
F7what this gene does

The F7 gene helps produce a protein important for blood clotting, which stops bleeding when dogs get injured.

For your dog: If your dog is from a breed known to carry F7 variants, it's worth mentioning to your vet before any surgery or if you notice unusual bleeding.

Fanconi Syndrome
Autosomal recessive
low <0.1%
n = 5,153 dogs · 1 variant tested · OMIA:000366-9615 · omia.org →
Amelogenesis Imperfecta (Discovered in the Parson Russell Terrier; AI)
Autosomal recessive
low <0.1%
n = 5,154 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.

Early-Onset Progressive Polyneuropathy (Discovered in the Greyhound)
Autosomal recessive
low <0.1%
n = 5,154 dogs · 2 variants tested · OMIA:002120-9615 · omia.org →
NDRG1what this gene does

NDRG1 is a gene involved in nerve cell function and maintenance, helping keep the nervous system working properly.

For your dog: If your dog is from a breed known to carry NDRG1 variants, it’s worth discussing with your vet, especially if you notice any mobility issues.

Episodic Falling (EF)
Autosomal recessive
Pathogenic low <0.1%
n = 5,154 dogs · 1 variant tested · OMIA:001592-9615 · omia.org →
Show the other 5, ordered after these by severity, then carrier frequency.
Hereditary Footpad Hyperkeratosis (Discovered in the Irish Terrier and Kromfohrländer) <0.1% n = 5,154
Macrothrombocytopenia (Discovered in the Norfolk and Cairn Terrier) <0.1% n = 5,154
Musladin-Lueke syndrome (MLS) <0.1% n = 5,154
Prekallikrein Deficiency <0.1% n = 5,154
Pyruvate Kinase (PK) Deficiency (Discovered in the Beagle) <0.1% n = 5,154
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: 5,154 dogs from the Donner 2023 cohort.
In plain terms

What these results mean for a Pug

Degenerative myelopathy (DM)

26.0% of Pugs in the Donner 2023 cohort carried it (n=5,154).

  • 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.

Chondrodystrophy and disc disease risk (CDDY)

1.5% of Pugs in the Donner 2023 cohort carried it (n=5,136).

  • 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.

Which Mendelian variants matter most for Pugs?

The Mendelian-disease table above lists 25 variants at observable carrier frequency, from 194 variants screened in 5,154 Pugs (Donner 2023). Two matter most by carrier frequency and clinical impact.

Von Willebrand’s Disease, Type 1 (vWD 1)

Von Willebrand’s disease Type 1 in Pugs is an autosomal-recessive bleeding disorder caused by low levels of von Willebrand factor. Affected dogs have prolonged bleeding after trauma or surgery. 2.1% of Pugs carry the variant (n=5,154). The penetrance is low: Donner S4 confirmed phenotype in only 6/33 at-risk dogs (maximum 18% penetrance).

Testing is available. Affected dogs are managed through surgical precautions and transfusion support if needed.

How should I test my Pug?

A breed-specific panel from a CLIA-accredited lab is the high-yield path. The minimum useful set for Pugs is degenerative myelopathy (DM), CDDY (chondrodystrophy/IVDD), von Willebrand’s disease Type 1, and cone-rod dystrophy (crd4). These four cover the highest-frequency and highest-impact variants in the breed.

What should I feed a Pug?

Feeding a Pug well means feeding around the breed’s brachycephalic anatomy and high baseline intervertebral disc disease risk. Pugs cannot pant efficiently, which means heat-of-the-day exercise is dangerous and meal timing matters more than it does for most breeds. Add to that the breed’s near-universal CDDY variant carriage and high degenerative myelopathy carrier frequency (26.0%, n=5,154), and spinal health becomes a primary nutritional priority.

Heat management drives meal timing. Pugs overheat faster than longer-muzzled breeds because they cannot cool themselves through evaporative panting. Feed the main meal in the cool morning or evening, not midday. Small, frequent meals are safer than one large meal, which increases abdominal pressure and disc stress.

Joint and spinal support matters for a compact, heavy-fronted breed. Only about 1.5% of Pugs carry the CDDY variant that predisposes to IVDD (Donner 2023, n=5,154), so this is about body condition, not a variant every Pug has. An adult formulation with glucosamine, chondroitin, and omega-3 fatty acids is evidence-based support. A large body of peer-reviewed literature (including ACVIM guidelines on joint disease) supports these supplements in breeds at risk for degenerative joint disease and disc herniation. Maintain lean body condition aggressively: a Pug at ideal weight has better spinal support than an overweight one, and excess weight accelerates disc degeneration.

Protein adequacy and taurine sufficiency prevent secondary problems. Pugs with degenerative myelopathy (26% carrier frequency) benefit from adequate dietary protein and muscle-sparing during the symptomatic phase. A minimum of 18% crude protein in adult food is the NRC 2006 standard for adult maintenance; for Pugs with DM risk or progression, 22-25% is appropriate. Taurine supplementation is not contraindicated in Pugs. Cardiac support is a reasonable goal in a small-breed dog, though breed-specific mitral valve disease prevalence data for Pugs is not established in the Donner 2023 dataset. Standard commercial foods designed for toy breeds typically meet these targets, but verify the label.

What we don’t know

The honest summary is that we do not know which Pugs in the 26% degenerative myelopathy carrier pool become symptomatic and which do not. Donner 2023 does not publish a penetrance fraction for DM in Pugs specifically. The gap between the 26% carrier frequency and observed symptomatic cases suggests incomplete penetrance, but the degree is not yet quantified for this breed. That gap means environmental and polygenic modifiers are at work, but they are not yet mapped. Age of onset also varies widely in published case reports; symptomatic dogs in the literature present anywhere from middle age to late life.

The relationship between heat stress and IVDD symptom progression in Pugs specifically has not been formally studied. Brachycephalic overheating is well-documented (Packer et al. 2012, BMC Veterinary Research). Anecdotal owner reports link heat exposure to acute disc herniation in Pugs. We do not yet have prospective data isolating that causal link in this breed.

Frequently asked questions about Pugs

What is the most common genetic disease in Pugs? Degenerative myelopathy. 26.0% of Pugs carry the variant (Donner 2023, n=5,154), though not all carriers become symptomatic due to incomplete penetrance.

Are Pugs prone to back problems? Spinal problems are reported in Pugs, but the CDDY variant is uncommon in the breed: about 1.5% carry it (Donner 2023, n=5,154). Avoid jumping, sustained running, and rapid weight gain. Lean body condition and spinal support (glucosamine, chondroitin, omega-3) are the owner’s primary levers.

How long do Pugs typically live? Cited life expectancy is 11.6 years (McMillan 2024 / VetCompass, n=10,026, 95% CI 11.4 to 11.8). Some individual Pugs exceed the median, though published lifespan data beyond the atlas figure is limited.

Should I do a DNA test on my Pug? For breeding stock, yes. For pet Pugs, testing helps you identify degenerative myelopathy and von Willebrand’s disease carriers so you can plan preventive care and manage breeding decisions if you ever choose to breed.

Can Pugs handle heat and exercise? Pugs are brachycephalic and overheat easily. Exercise should be short, low-intensity, and in cool parts of the day. Avoid strenuous play in warm weather. Their anatomy does not permit the thermoregulation that longer-muzzled breeds have.

What do I feed a Pug with degenerative myelopathy? There is no cure, but nutrition supports quality of life. Maintain lean body condition to reduce spinal load. Use a diet with adequate protein (22-25% crude protein), glucosamine, and omega-3 fatty acids. Consult your veterinarian about pharmaceutical support as symptoms progress.

Is Von Willebrand’s disease a serious problem in Pugs? It can be. The variant is autosomal recessive with low penetrance (confirmed in only 18% of at-risk dogs), so many carriers are asymptomatic. Affected dogs have prolonged bleeding after injury or surgery. Inform your veterinarian if your Pug is a carrier before any procedure.

Do Pugs need special nutrition as puppies? Toy-breed puppy formulations are appropriate. Transition to an adult toy-breed formulation by around one year of age, following the food manufacturer’s or your veterinarian’s guidance. Avoid overfeeding: excess weight in puppyhood increases joint and spinal stress later.

Temperament

What Pugs tend toward

Tendencies from owner surveys of purebred Pugs — 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
Biddabilitybreed ~18%
biddableindependent
Agonistic Thresholdbreed ~9%
assertivediffident
n = 27 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 Pug is also recorded as Carlin, Chinese pug, Dutch bulldog, Dutch mastiff, Mini mastiff, and Mops.

Identified as Pug (VBO:0201089) in the Vertebrate Breed Ontology (Mullen et al. 2025, CC-BY 4.0) · registry IDs FCI 253 · iDog 196 · VeNom 14599.

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

In the atlas, the Pug clusters consistently as Pug (100% of the 31 dogs here). Dogs here sit in a relatively sparse region of the atlas, fewer close neighbors than typical.

Ranks 16 of 107 on the bottleneck severity scale, well into the upper quartile of population contraction.

Median lifespan is 11.5 years, slightly shorter than expected for the breed size (7.25 kg).

Genetic dimensions · CanVAS atlas

What the atlas genotypes say about Pug

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
18 from Hayward2016, 10 from Spatola, 3 from JenkinsWGS
Genetic diversity
0.25Tight
Mean heterozygosity across the breed. 16th tightest 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: 22.54 · 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
Gave rise to
Close cousins
In the Toy 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
11.6years (life expectancy)
95% CI 11.4–11.8 · VetCompass, McMillan 2024, n=10,026. 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

Pugs are a natural model for human disease

Because the same genes cause the same conditions across species, the inherited conditions documented in Pugs 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.

  • amyotrophic lateral sclerosis type 1, modeled by the breed's Degenerative myelopathy via SOD1, the same underlying biology.
  • OMIM:603165, modeled by the breed's Dermatitis, atopic , the same underlying biology.
  • macrothrombocytopenia and granulocyte inclusions with or without nephritis or sensorineural hearing loss, modeled by the breed's May-Hegglin anomaly , the same underlying biology.
  • myelodysplastic syndrome, modeled by the breed's Myelodysplastic syndrome , the same underlying biology.
  • pyruvate kinase deficiency of red cells, modeled by the breed's Pyruvate kinase deficiency of erythrocyte , the same underlying biology.
  • OMIM:602151, modeled by the breed's Screw tail , the same underlying biology.
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 Pug

Beyond the testable carriers above, OMIA's literature catalogue records 13 genetic conditions in the Pug, 9 of which have a known human equivalent. This is the documented landscape across all Pugs 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