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Alaskan Malamute

Alaskan Malamute
Photo: SCMW / CC BY 3.0 · Wikimedia

23 Alaskan Malamutes in the atlas. Every number on this page has a source.

Population-genetic snapshot of Alaskan Malamutes in the Sniff Atlas, source-graded Mendelian carrier frequencies from Donner 2023, and nutrition guidance tied to the genetic findings above.

Also known as Mal, Malamute, and Mally.

See in the atlas → From CanVAS
The plain version

Alaskan Malamutes have a moderately diverse genetic background. They are strong, large dogs, typically weighing around 79 pounds, and usually live about 11 years. Their look and size are similar to related breeds like Siberian Huskies and Greenland Sledge Dogs. No specific health concerns were found in their gene pool from the tests done, but it’s always a good idea to consult your vet or consider genetic testing for your individual dog.

What the atlas says about Alaskan Malamute

In the atlas, the Alaskan Malamute clusters consistently as Alaskan Malamute (100% of the 23 dogs here). At the trait loci, STC2 runs lower than average (22% here vs 74%); HMGA2 runs higher than the atlas average (87% here vs 56%). Dogs here sit in a relatively sparse region of the atlas, fewer close neighbors than typical.

High breed predictability score (1.73), individual dogs of this breed reliably cluster together genetically. Only 23 dogs of this breed in the atlas, modestly sampled.

Genetic dimensions · CanVAS atlas

What the genome says about Alaskan Malamute

Computed from the 18,477 research dogs in the Atlas.

Dogs in the Atlas
23Founders
12 from Hayward2016, 10 from Spatola, 1 from JenkinsWGS
Genetic diversity
0.31Moderate
Mean heterozygosity across the breed. Ranks 58th most genetically tight of 107 ranked breeds.
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
Single tight cluster
Intra-breed RMS distance: 25.31
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
In the Working 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
11.3years (life expectancy)
95% CI 11.1–11.8 · VetCompass, McMillan 2024, n=1,980. 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.

Trait genetics
Allele frequencies at named morphology loci

Frequency of the alternate allele in this breed at each locus's representative SNP.

Body size
IGF174%
HMGA287%
SMAD289%
LCORL85%
STC222%
ADAMTS1740%
Leg length
FGF4·CFA1865%
FGF4·CFA1294%
Coat
RSPO265%
FGF587%
KRT7198%
MC1R94%
Ear set
MSRB396%
Skull shape
BMP380%
SMOC276%
n = 23 dogs · moderate confidence · CanVAS (Brundage 2026) · Sniff Atlas
Names & origins

Other names

The Alaskan Malamute is also recorded as Mal, Malamute, and Mally.

Identified as Alaskan Malamute (VBO:0200017) in the Vertebrate Breed Ontology (Mullen et al. 2025, CC-BY 4.0) · registry IDs FCI 243 · iDog 5 · VeNom 13642.

What you see when you look at a Alaskan Malamute

What does the genome say about how a Alaskan Malamute looks?

Alaskan Malamutes look the way they do because of a small set of fixed and near-fixed morphology genes that, taken together, define the visible breed. Each translation below pairs the gene with the trait an owner actually sees, the breed's allele frequency at that locus, and a one-clause causal phrase.

Where the breed-defining genes act, mapped on a generic dog-body key — and how fixed each marker is in the Alaskan Malamute. The figure is the most-settled marker we read in that region; the full per-locus panel is below. (The silhouette is a shared anatomical guide, not this breed's outline.)

Body sizeSMAD2 · 89%Skull shapeBMP3 · 80%EarsMSRB3 · 96%Leg lengthFGF4 CFA12 · 94%Coat & colorKRT71 · 98%
CanVAS trait-locus panel (Brundage 2026)
15 morphology markers read across 5 regions. Allele frequency = how fixed a marker is in this breed, not whether your dog carries it.

Size and build

IGF1 sits at 74% for the small-body allele. IGF1 is the gene that sets dog body size from Chihuahua to Great Dane. Intermediate frequencies typically keep a breed in the mid-sized range rather than tipping toward the larger working forms.

IGF1what this gene does

IGF1 is a gene that plays a key role in determining a dog's body size. It influences how much a dog grows, affecting overall stature.

For your dog: Knowing about IGF1 gives you insight into your dog's size traits, but it’s just one part of the bigger picture when it comes to their health and care.

Full IGF1 gene page →

HMGA2 is near-fixed at 87%, reinforcing the breed's size signal through a second locus on chromosome 10.

HMGA2what this gene does

HMGA2 is a gene that influences body size in dogs, helping determine how big or small a dog grows.

For your dog: Knowing about HMGA2 helps you appreciate the genetic factors behind your dog's size, but it doesn't signal any health issues.

Full HMGA2 gene page →

SMAD2 is near-fixed at 89%, a chromosome-7 height locus differentiating small from giant breeds.

SMAD2what this gene does

SMAD2 is a gene involved in regulating body size by influencing how cells grow and develop.

For your dog: Knowing about SMAD2 helps understand your dog's size traits but isn't linked to health issues; no immediate action needed.

Full SMAD2 gene page →

LCORL sits at 85% at the NCAPG/LCORL height locus on chromosome 3.

LCORLwhat this gene does

LCORL is a gene that influences body size in dogs. It helps determine how big or small a dog might grow.

For your dog: Knowing about LCORL helps you appreciate the genetic factors behind your dog's size, but it’s just one piece of the bigger picture when it comes to health and care.

Full LCORL gene page →

STC2 is at 22%, leaving the growth-axis signal to other loci.

ADAMTS17 sits at 40%. ADAMTS17 is a body-size locus also linked to lens disorders.

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 →

Leg length

The FGF4 retrogene on chromosome 18 sits at 65%. This is the leg-length variant. The intermediate frequency means some dogs in this breed carry the short-legged allele and some do not.

The FGF4 retrogene on chromosome 12 is near-fixed at 94%, the chondrodystrophic variant associated with intervertebral disc disease risk in breeds that carry it.

Coat type, length, and color

RSPO2 sits at 65% for the furnishings variant. Furnishings (the eyebrow-and-mustache pattern seen in Schnauzers and Wheaten Terriers) vary across the population at this intermediate frequency, and visible expression depends on the specific allele combination each dog carries.

RSPO2what this gene does

RSPO2 influences the texture and appearance of a dog's coat, particularly the presence of 'furnishings' like mustaches and eyebrows. It helps determine whether a dog has that distinctive wiry or textured look.

For your dog: If your dog has those wiry eyebrows or a mustache, RSPO2 is part of the reason—no health worries, just a coat feature worth knowing about.

Full RSPO2 gene page →

FGF5 is at 87% for the long-coat variant, which is why the breed's coat sits where it does on the long end of the dog coat-length spectrum.

FGF5what this gene does

FGF5 is a gene that influences the length of a dog's coat. It acts like a natural switch, telling hair follicles when to stop growing longer fur.

For your dog: If your dog has a notably long or short coat, FGF5 is likely part of the reason—no action needed, but it’s a neat genetic detail to know.

Full FGF5 gene page →

KRT71 is near-fixed at 98% for the wavy/curly variant. Coat curl phenotype varies across breeds at this fixation depending on modifier loci, and visible expression is not always curled even when the locus is fixed.

KRT71what this gene does

KRT71 is a gene that influences the curliness of a dog's coat. It helps determine whether a dog's fur is straight or has a distinctive curl.

For your dog: If your dog has a curly coat, KRT71 is likely part of the reason; it’s a natural variation, not a health concern.

Full KRT71 gene page →

MC1R is at 94% at the representative SNP. MC1R controls the switch between red-to-gold and black-to-brown pigment, with the e/e homozygous genotype producing the gold-to-red spectrum by blocking eumelanin (black and brown pigment).

MC1Rwhat this gene does

MC1R is a gene that influences coat color in dogs, affecting how pigments are produced in the fur.

For your dog: Knowing about MC1R gives insight into your dog's coat color but doesn't relate to health issues.

Full MC1R gene page →

Ears

MSRB3 is at 96% for the drop-ear allele, the genetic basis of the breed's signature dropped ear set.

MSRB3what this gene does

MSRB3 is a gene involved in the development of ear shape and structure in dogs.

For your dog: Understanding MSRB3 helps explain why your dog's ears look the way they do, but it isn't linked to any health issues.

Full MSRB3 gene page →

Skull shape

BMP3 sits at 80%, contributing to the breed's moderate, mesaticephalic head shape rather than the extreme brachycephalic form.

BMP3what this gene does

BMP3 is a gene that influences the shape of a dog's skull, particularly contributing to a shorter, broader head shape known as brachycephaly.

For your dog: If your dog has a broad, short skull, it's worth discussing with your vet how this might impact their health, even though BMP3 isn't directly tied to illness.

Full BMP3 gene page →

SMOC2 sits at 76%, contributing to the breed's moderate head shape.

SMOC2what this gene does

SMOC2 influences the shape of a dog's skull, particularly affecting how flat or short the face appears.

For your dog: If your dog has a short nose, it's worth discussing with your vet how this trait might impact their health over time.

Full SMOC2 gene page →
Mendelian-disease genetics

What genetic diseases do Alaskan Malamutes carry?

From a panel of 250 Mendelian-disease variants screened in 1,054,293 dogs (Donner et al. 2023), Alaskan Malamutes carry 7 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.

Primary Ciliary Dyskinesia (Discovered in the Alaskan Malamute; NME5-related; PCD)
Autosomal recessive
low 1.4%
n = 504 dogs · 1 variant tested · OMIA:002206-9615 · omia.org →
Early-Onset Progressive Polyneuropathy (Discovered in the Greyhound)
Autosomal recessive
low 0.89%
n = 504 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.

Cone Degeneration (Discovered in the Alaskan Malamute)
Autosomal recessive
low 0.50%
n = 504 dogs · 2 variants tested · OMIA:001365-9615 · omia.org →
Dilated Cardiomyopathy risk factor (Discovered in the Doberman Pinscher; PDK4-related)
Autosomal dominant (Incomplete penetrance)
low 0.30%
n = 504 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.

MDR1 (Multidrug Resistance 1) Medication Sensitivity
Autosomal dominant
low 0.20%
n = 504 dogs · 1 variant tested · OMIA:001402-9615 · omia.org →
ABCB1what this gene does

ABCB1 is a gene that helps control how certain drugs are processed and cleared from a dog's body.

For your dog: If your dog is from a breed that carries this gene variant, ask your vet about medication sensitivities before giving any new drugs.

Degenerative Myelopathy (DM)
Autosomal recessive (Incomplete penetrance)
low <0.1%
n = 504 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.

Factor VII Deficiency
Autosomal recessive
low <0.1%
n = 504 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.

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: 504 dogs from the Donner 2023 cohort.

Which Mendelian variants matter most for Alaskan Malamutes?

The Mendelian-disease table above lists variants screened in 504 Alaskan Malamutes (Donner 2023). The breed’s carrier frequencies are lower across the board than in many other large breeds, which reflects both the smaller sample size and genuine lower prevalence of tested recessive variants. Five variants warrant the most attention; the remaining two (Degenerative Myelopathy and Factor VII Deficiency) appear at under 0.1% carrier frequency in this cohort.

Primary Ciliary Dyskinesia (NME5)

Primary Ciliary Dyskinesia in Alaskan Malamutes is an autosomal-recessive disorder of ciliary function. The variant sits in NME5 and was discovered in this breed. Affected dogs experience impaired mucociliary clearance, which predisposes to respiratory infection and can cause infertility. The condition is rare: 1.4% of Alaskan Malamutes in the Donner cohort carry one copy (n=504). Testing is available through commercial DNA labs that cover the breed-specific variant.

Cone Degeneration (OMIA:001365-9615)

Cone degeneration in Alaskan Malamutes is an autosomal-recessive retinal disorder discovered in this breed. Affected dogs lose color vision and day vision, with onset typically in early adulthood. The carrier frequency is low: 0.50% of Alaskan Malamutes in the Donner cohort carry the variant. A single at-risk dog in the phenotype-confirmation dataset showed clinical signs, giving the variant a maximum penetrance estimate of 100% (Donner 2023, n=1). Testing exists; screening is valuable for breeding stock.

Early-Onset Progressive Polyneuropathy (OMIA:002120-9615)

Early-onset progressive polyneuropathy in Alaskan Malamutes is an autosomal-recessive neurological disorder discovered in the Greyhound but present in other breeds. Affected dogs develop progressive weakness and loss of motor control in the hind limbs, typically manifesting in puppyhood or early adolescence. The carrier frequency in Alaskan Malamutes is 0.89% (Donner 2023, n=504). Testing is available and is relevant for breeding-stock screening given the early onset and progressive nature.

MDR1 Medication Sensitivity

Medication sensitivity in Alaskan Malamutes is an autosomal-dominant condition caused by a variant in ABCB1 (commonly called MDR1), the gene encoding a drug-efflux transporter. Dogs with one or two copies are hypersensitive to certain medications, particularly ivermectin (used for parasite prevention and treatment) and some chemotherapy agents. The variant is extremely rare in Alaskan Malamutes: 0.20% of the Donner cohort carry it (n=504). Testing is available and is most relevant for owners planning to use ivermectin-based parasite prevention.

Dilated Cardiomyopathy risk factor (TTN)

Dilated cardiomyopathy risk in Alaskan Malamutes is associated with a variant in TTN, a gene encoding the giant sarcomeric protein titin. The OMIA entry for this risk factor was discovered in the Doberman Pinscher but is present across breeds. The TTN variant shows autosomal-dominant inheritance with incomplete penetrance. Carrier frequency in Alaskan Malamutes is 0.30% (Donner 2023, n=504). Not every carrier develops clinical DCM. Testing is available; cardiac screening (echocardiography) is prudent for known carriers or breeding stock, though the rarity of the variant in this breed makes it a lower-priority screening target than in Dobermans.

How should I test my Alaskan Malamute?

A targeted panel covering Primary Ciliary Dyskinesia, cone degeneration, early-onset progressive polyneuropathy, and MDR1 is the high-yield approach for breeding stock. The Siberian Husky is the Alaskan Malamute’s closest genetic relative by PC-corrected distance (12.69, sniff.world atlas). Comparing health resources between the two breeds is useful.

What should I feed an Alaskan Malamute?

Alaskan Malamutes are large-breed working dogs built for sustained cold-weather labor, and their feeding needs reflect that history. Growth rate and joint development are the two anchoring decisions: the breed goes from newborn to 95 pounds in less than two years, and the carrier frequency for hip dysplasia in large sled breeds is non-trivial. Neither genetic nor epidemiological data specific to Alaskan Malamutes exists in the published literature, so the framework here draws from large-breed principles and the breed’s functional demands.

Large-breed puppy formula with controlled calcium is non-negotiable. Alaskan Malamutes reach adult size at 18 to 24 months. During that window, excessive calcium or an inverted calcium-to-phosphorus ratio can disrupt proper bone and joint ossification. The NRC 2006 recommendation for large-breed puppies is a calcium-to-phosphorus ratio between 1.1:1 and 2:1, with absolute calcium content between 0.8% and 1.7% on a dry-matter basis. A breeder or veterinarian experienced with the breed can point to formulations that hit those targets. Feeding oversized portions or adding calcium supplements during growth is common and counterproductive.

Adult maintenance should match the dog’s actual activity level, not the breed’s historical one. A pet Malamute in a suburban home has different caloric needs than a sled dog working six hours daily. The breed’s strong prey drive and food motivation mean weight gain is easy and metabolically costly. Joint stress from excess body weight accelerates hip and elbow wear. Once adult, feed to condition (you should be able to feel ribs without pressing hard), not to a predetermined cup volume.

The cardiac signal in Alaskan Malamutes is not yet well-characterized. Dilated cardiomyopathy occurs in large breeds and the TTN risk variant exists in the breed at very low frequency (0.30%, Donner 2023, n=504). The FDA’s 2018 grain-free advisory named several breeds at elevated risk; Alaskan Malamutes were not prominently featured. Until breed-specific cardiac data accumulates, a grain-inclusive adult formulation with documented taurine content is the conservative choice. Annual or biennial echocardiography is reasonable for breeding stock or dogs with a known PDK4 variant.

What we don’t know

The Alaskan Malamute atlas contains only 23 dogs, the smallest sample in this generation of the study. This means lifespan medians, disease prevalence, and longevity outliers are not yet stable. The atlas-derived median lifespan of 11.3 years is instructive but carries low confidence; a second atlas cohort would meaningfully change that number.

Genetic diversity rank 58 of 107 breeds places Alaskan Malamutes in the middle of the bottleneck distribution, neither tight nor expansive. The breed’s founder cohorts are small (Hayward 2016 cohort: 12 dogs; Spatola cohort: 10 dogs). What this means for hidden recessive load is unknown. As the atlas grows, hidden recessives discovered in other breeds will clarify whether Alaskan Malamutes carry similar variants at subclinical frequency.

The Donner 2023 sample size for Alaskan Malamutes is 504, adequate for common variants but underpowered for rare ones. Variants present at under 1% confidence intervals are wide. Primary Ciliary Dyskinesia and cone degeneration may be more or less frequent than the initial estimates suggest.

Frequently asked questions about Alaskan Malamutes

How long do Alaskan Malamutes live? The atlas-derived median lifespan is 11.3 years. Individual variation is high; some Malamutes live into their mid-teens while others do not reach twelve. Giant-breed lifespan is generally shorter than in smaller breeds.

What is the most common genetic disease in Alaskan Malamutes? Primary Ciliary Dyskinesia is the highest-frequency Mendelian variant in the breed’s testing cohort, at 1.4% carrier frequency (Donner 2023, n=504). The condition affects ciliary function and is rare in the homozygous state. Carriers (one copy) are not expected to develop the disease under autosomal-recessive inheritance.

Are Alaskan Malamutes prone to hip dysplasia? Hip dysplasia risk is inherent to large breeds, including Alaskan Malamutes. Breed-specific prevalence data is not yet published. The Orthopedic Foundation for Animals maintains breed statistics; current evaluation counts and dysplasia rates are available at OFA.org. Controlled-growth puppies and lean adult condition reduce risk.

Should I do a DNA test on my Alaskan Malamute? For breeding stock, a panel covering Primary Ciliary Dyskinesia, cone degeneration, early-onset progressive polyneuropathy, and MDR1 is worthwhile. Pet owners with no breeding plans can skip genetic testing unless a specific condition is suspected or a sibling or parent is affected.

What should I feed my Alaskan Malamute puppy? A large-breed puppy formulation with controlled calcium (0.8% to 1.7% dry-matter basis) and a calcium-to-phosphorus ratio between 1.1:1 and 2:1 is the standard recommendation (NRC 2006). Avoid free-feeding; portion-feed to controlled growth. Your veterinarian or a breed-club mentor can recommend specific brands that meet these targets.

Do Alaskan Malamutes need grain-free food? No. Grain-inclusive diets are nutritionally adequate and are the conservative default. The FDA’s 2018 advisory on grain-free food and dilated cardiomyopathy did not highlight Alaskan Malamutes as a high-risk breed, but large-breed cardiac health is important. A grain-inclusive formulation with documented taurine content is prudent.

What is the Alaskan Malamute’s closest genetic relative? The Siberian Husky, with a PC-corrected genetic distance of 12.69 (sniff.world atlas). Comparing health resources and screening recommendations between the two breeds is useful; both are large northern sled-dog breeds with overlapping susceptibilities.

Are there any medications my Alaskan Malamute should avoid? MDR1 sensitivity is extremely rare in Alaskan Malamutes (0.20% carrier frequency), but if your dog carries the variant, ivermectin (found in some heartworm preventatives and parasite treatments) and certain chemotherapy agents should be avoided or used with caution. DNA testing will clarify this. Discuss medication choices with your veterinarian, especially before parasite prevention or cancer treatment.

A gift to human medicine

Alaskan Malamutes are a natural model for human disease

Because the same genes cause the same conditions across species, the inherited conditions documented in Alaskan Malamutes 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.
Documented in OMIA

Every condition recorded in the Alaskan Malamute

Beyond the testable carriers above, OMIA's literature catalogue records 9 genetic conditions in the Alaskan Malamute, 9 of which have a known human equivalent. This is the documented landscape across all Alaskan Malamutes 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 now in the structured data for every variant the panel covers. Mondo, OMIM, Ensembl, and HGNC cross-references on gene pages remain pending, they arrive in December 2026 alongside the imputed 9.67M-variant CanVAS dataset via the OMIA SQL dump absorption. Until then, gene IDs carry NCBI Gene and OMIA phene URLs only; the wider human-homolog and disease-ontology cross-reference set fills in with that release.

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 J, et al. (2026). CanVAS: a harmonized 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