Saluki
Salukis have a cited life expectancy of 13.3 years (McMillan 2024 / VetCompass, n=428, 95% CI 12.3 to 14). The most carried tested variant is Hereditary Nasal Parakeratosis, in 4.2% of 24 Salukis tested (Donner 2023), then Cone-Rod Dystrophy (2.1%). 26 dogs stand behind the atlas figures here, so treat this page as an early sketch.
Also known as Persian Greyhound, Tanji, and Tazi.
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.
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.
For researchers Population genetics, disease models and every recorded condition Open the research detail for the Saluki
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.
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 atlas genotypes say about Saluki
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.
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.
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 via CLN8, 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 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.
Some things about living with a saluki never make it into a database. Add what you know as a Keeper, in your words →
Lived experience, kept beside the science.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 DM (2026). CanVAS: A Harmonized and Imputed 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).