Sealyham Terrier
Only 4 Sealyham Terriers have been tested for disease variants (Donner 2023), too few to say which variants the breed has.
Which disease variants turn up in Sealyham Terriers?
From a panel of 250 Mendelian-disease variants screened in 1,054,293 dogs (Donner et al. 2023), 4 turn up in Sealyham Terriers at observable frequency. The figure beside each is its allele frequency. Of the gene copies tested in this breed, the share that carry the variant. Every dog carries two copies, so this is not the share of dogs. It 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.
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.
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.
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.
What these results mean for a Sealyham Terrier
About 75 in every 100 copies of this gene in the 4 Sealyham Terriers tested carry this change (Donner 2023).
- Extra copies of a growth gene called FGF4 shape a dog's legs and back. The copy on chromosome 12 is the one linked to disc disease. The copy on chromosome 18 makes legs shorter.
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 the risk, but it can't tell you which dog will have a disc problem. In Dachshunds, researchers found the test on its own isn't a reliable guide.
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 vet what the result means for your dog. The sources here don't say what lowers the risk for a dog that carries it.
Not tested, or a mix
Without a test, no one can tell. Short legs don't tell you either: the disc copy and the short-leg copy are different.
About 25 in every 100 copies of this gene in the 4 Sealyham Terriers tested carry this change (Donner 2023).
- DM slowly damages the spinal cord in adult dogs, until the back legs stop working. Nothing yet can stop 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 gene change mean a dog is at risk, not that it will get sick. Some dogs with two copies never do.
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 this change, every dog with DM that was tested had two copies.
OMIA 000263-9615
“All affected dogs tested were homozygous mutant.” OMIA 000263-9615
What to do
A DNA result isn't a diagnosis. If the way your dog walks changes, take that and the result to your vet.
Not tested, or a mix
Without a test, no one can tell how many copies your dog has. How common it is in a breed says nothing about one dog.
A heart (DCM) test that doesn't hold up
Not a reliable testAbout 25 in every 100 copies of this gene in the 4 Sealyham Terriers tested carry this change (Donner 2023).
- This gene change was linked to a heart disease called DCM in Dobermans, but it hasn't been shown to cause it. The curated record says a test for it isn't a good guide to heart risk, even in Dobermans.
OMIA 000162-9615
“it is evident that any DNA test based on this marker will not be a good indicator of liability to this disorder in Dobermans” OMIA 000162-9615
What to do
A result for this one isn't, by itself, a reason for heart tests. Whether to check your dog's heart is a conversation to have with your vet.
Not tested, or a mix
Outside the Doberman, no one has shown what this change means.
For researchers Population genetics, disease models and every recorded condition Open the research detail for the Sealyham Terrier
Where every number on this page came from.
This page draws on one primary data source. Allele frequencies and sample sizes come from Donner et al. 2023 (CC-BY-4.0), a direct-to-consumer screening cohort, graded Limited as a study design because the dogs were tested at their owners' choice. No genotyped research dogs of this breed are in the three open releases the atlas reads, so the population-genetic sections other breed pages carry are absent here for that reason, not hidden. Conditions recorded for the breed come from OMIA.
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. Cite Donner et al. 2023 (doi:10.1371/journal.pgen.1010651) for every frequency on this page, and OMIA for each condition, with the sample size shown beside the figure.
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- 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).