Saluki
26 Salukis in the atlas. Every number on this page has a source.
26 Salukis in the Sniff Atlas. Population-genetic snapshot, Mendelian carrier frequencies from Donner 2023, and the data substrate's release version, sample sizes, and evidence tier on every claim.
Also known as Persian Greyhound, Tanji, and Tazi.
Salukis have a moderately diverse genetic background, which means they have a healthy mix of traits within the breed. They’re a graceful, medium-sized dog, typically weighing around 50 pounds, and usually live about 13 years. One health note to keep in mind is Bald Thigh Syndrome, a condition found in the breed’s gene pool; this doesn’t mean every Saluki will have it, but it’s a good idea to talk with your vet or consider genetic testing to stay informed. Overall, they’re a lovely, well-balanced breed with close ties to Afghan Hounds and Taigans.
In the atlas, the Saluki clusters consistently as Saluki (100% of the 26 dogs here). Genetic diversity is high (mean heterozygosity 0.3499), reflecting either a mixed-breed cluster or breeds with broad genetic backgrounds. At the trait loci, HMGA2 runs higher than the atlas average (90% here vs 56%); STC2 runs lower than average (42% here vs 74%).
Ranks 87 of 107 on the bottleneck severity scale, in the upper quartile of genetic diversity. Mean heterozygosity is 0.350, notably high, indicates broad genetic background. Only 26 dogs of this breed in the atlas, modestly sampled.
Median lifespan is 13.3 years, slightly longer than expected for the breed size (22.5 kg).
What the genome says about Saluki
Computed from the 18,477 research dogs in the Atlas.
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.
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.
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.
Frequency of the alternate allele in this breed at each locus's representative SNP.
| IGF1 | 84% |
| HMGA2 | 90% |
| SMAD2 | 79% |
| LCORL | 90% |
| STC2 | 43% |
| ADAMTS17 | 64% |
| FGF4·CFA18 | 87% |
| FGF4·CFA12 | 92% |
| RSPO2 | 67% |
| FGF5 | 75% |
| KRT71 | 60% |
| MC1R | 89% |
| MSRB3 | 67% |
| BMP3 | 62% |
| SMOC2 | 92% |
Other names
The Saluki is also recorded as Persian Greyhound, Tanji, and Tazi.
Identified as Saluki (VBO:0201171) in the Vertebrate Breed Ontology (Mullen et al. 2025, CC-BY 4.0) · registry IDs FCI 269 · iDog 209 · VeNom 14646.
What does the genome say about how a Saluki looks?
Salukis 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 Saluki. 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.)
Size and build
IGF1 sits at 84% 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 90%, 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 sits at 79% at the chromosome-7 height locus.
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 is near-fixed at 90%, the NCAPG/LCORL height locus that is one of the strongest single contributors to canine body size.
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 sits at 43%.
ADAMTS17 sits at 64%. 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 is near-fixed in this breed at 87%. This is the leg-length variant. The breed is fully committed to the long-legged form rather than the short-legged Corgi-and-Dachshund body plan.
The FGF4 retrogene on chromosome 12 is near-fixed at 92%, the chondrodystrophic variant associated with intervertebral disc disease risk in breeds that carry it.
Coat type, length, and color
RSPO2 sits at 67% 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 sits at 75% for the long-coat variant. Coat length is influenced by other loci as well, so intermediate FGF5 frequencies do not always correspond to intermediate visible coat lengths.
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 sits at 60% for the wavy/curly variant. Coat curl varies across individuals at this intermediate frequency, and visible expression is also influenced by modifier loci.
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 89% 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 sits at 67% for the drop-ear allele, which is why ear set varies across the breed.
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 62%, 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 is at 92%, the major locus contributing to the breed's brachycephalic face 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 →What genetic diseases do Salukis carry?
From a panel of 250 Mendelian-disease variants screened in 1,054,293 dogs (Donner et al. 2023), Salukis carry 3 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.
IGFBP5what this gene does
IGFBP5 is a gene that helps regulate growth factors involved in tissue development and repair.
For your dog: If you have a sighthound, it’s worth mentioning IGFBP5-related risks to your vet, but being a carrier doesn’t mean your dog will develop the syndrome.
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.
Salukis are a natural model for human disease
Because the same genes cause the same conditions across species, the inherited conditions documented in Salukis 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.
- neuronal ceroid lipofuscinosis 8, modeled by the breed's Neuronal ceroid lipofuscinosis, 8, the same underlying biology.
- succinic semialdehyde dehydrogenase deficiency, modeled by the breed's Succinic semialdehyde dehydrogenase deficiency, the same underlying biology.
Every condition recorded in the Saluki
Beyond the testable carriers above, OMIA's literature catalogue records 2 genetic conditions in the Saluki, 2 of which have a known human equivalent. This is the documented landscape across all Salukis ever studied, not a prediction for any one dog.
- Neuronal ceroid lipofuscinosis, 8 Autosomal recessiveHuman equivalent: neuronal ceroid lipofuscinosis 8
- Succinic semialdehyde dehydrogenase deficiency Autosomal recessiveHuman equivalent: succinic semialdehyde dehydrogenase deficiency
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.
We have 26 salukis. We do not have yours.
Every saluki added sharpens the breed's genetic neighborhood. Enrollment is free. The data stays open. The star is permanent.
- 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
- Brundage J, et al. (2026). CanVAS: a harmonized canine variant atlas. bioRxiv. doi:10.64898/2026.04.13.718238
- 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).