Border Terrier
Border Terriers have a cited life expectancy of 14.2 years (McMillan 2024 / VetCompass, n=9,387, 95% CI 14.1 to 14.3). The most carried tested variant is Chondrodystrophy and Intervertebral Disc Disease Risk, in 1.4% of 71 Border Terriers tested (Donner 2023).
What genetic diseases do Border Terriers carry?
From a panel of 250 Mendelian-disease variants screened in 1,054,293 dogs (Donner et al. 2023), Border Terriers carry 2 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.
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.
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.
What these results mean for a Border Terrier
1.4% of Border Terriers in the Donner 2023 cohort carried it (n=71).
- 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.
SLC7A9 p.A217T (sold as a cystinuria test)
Marker disputed1.4% of Border Terriers in the Donner 2023 cohort carried it (n=71).
- The curated record finds no support for this variant causing cystinuria, and the researchers who studied it advise against using it as a test.
OMIA 001880-9615
“there appears to be no support for the variant to be causal” OMIA 001880-9615
“strongly recommend not to use "the variant in SLC7A9 as a test to predict the risk of developing cystinuria in male English bulldogs.” OMIA 001880-9615
What to do
A carrier result for this variant does not predict bladder stones. Straining to urinate or blood in the urine is a reason to see a veterinarian whatever a DNA test says.
No test, or a mix
The curated record gives no reason to test for this variant.
Identified as Border Terrier (VBO:0200194) in the Vertebrate Breed Ontology (Mullen et al. 2025, CC-BY 4.0) · registry IDs FCI 10 · iDog 44 · VeNom 14962.
For researchers Population genetics, disease models and every recorded condition Open the research detail for the Border Terrier
In the atlas, the Border Terrier clusters consistently as Border Terrier (100% of the 59 dogs here). Dogs here sit in a relatively sparse region of the atlas, fewer close neighbors than typical.
Ranks 18 of 107 on the bottleneck severity scale, well into the upper quartile of population contraction.
Median lifespan is 14.2 years, slightly longer than expected for the breed size (6.12 kg).
What the atlas genotypes say about Border 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.
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.
Border Terriers are a natural model for human disease
Because the same genes cause the same conditions across species, the inherited conditions documented in Border 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.
- glycogen storage disease due to GLUT2 deficiency, modeled by the breed's Fanconi syndrome , the same underlying biology.
Every condition recorded in the Border Terrier
Beyond the testable carriers above, OMIA's literature catalogue records 1 genetic conditions in the Border Terrier, 1 of which have a known human equivalent. This is the documented landscape across all Border Terriers ever studied, not a prediction for any one dog.
- Human equivalent: glycogen storage disease due to GLUT2 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 border terrier never make it into a database. Add what you know as a Keeper, in your words →
Lived experience, kept beside the science.We have 59 border terriers. We do not have yours.
Every border terrier 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).