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This guide explains four important groups of canine genetic tests in detail: MDR1/ABCB1 drug sensitivity, Degenerative Myelopathy (Exon 2) (DM/SOD1), progressive rod-cone degeneration (prcd-PRA/PRCD), and the FGF4 retrogene insertions associated with CDPA and CDDY/IVDD.
For each test we'll cover:
the gene and exact genetic variant;
the inheritance pattern;
what happens biologically when the variant is present;
the clinical signs an affected or susceptible dog may develop;
how the condition is diagnosed clinically;
available treatment or management;
what the result means for breeding decisions.
There is also an important practical point for breeders. At Animalabs, these widely requested tests are not sold only as isolated results. Our breed-specific canine genetic panels include this core group of tests together with additional genetic tests selected for the individual breed, with the complete breed-specific panel priced below €100. This means that a breeder searching for one well-known mutation can obtain a substantially broader genetic assessment from the same DNA sample.
The MDR1 dog test is one of the most clinically useful pharmacogenetic tests available in veterinary medicine. It does not test whether a dog currently has a disease. Instead, it identifies a genetic variant that can change the way the dog's body handles certain medications and can substantially increase susceptibility to adverse drug reactions.
The affected gene is ABCB1 (ATP Binding Cassette Subfamily B Member 1), historically referred to as MDR1. ABCB1 encodes P-glycoprotein (P-gp), an ATP-dependent membrane transporter expressed in several tissues, including the blood-brain barrier, intestinal epithelium, liver and kidneys.
At the blood-brain barrier, P-glycoprotein acts as an efflux pump. Its job is to transport certain xenobiotics and drugs out of cells and to restrict their accumulation within the central nervous system. When functional P-glycoprotein is absent or markedly reduced, substrates of this transporter can reach unexpectedly high concentrations in the brain.
The classic canine MDR1 variant is a four-base-pair deletion, commonly written as ABCB1:c.227_230delATAG and historically described as mdr1-1Δ or nt230(del4). The deletion causes a frameshift and introduces premature stop codons. The resulting protein is severely truncated rather than producing normal full-length P-glycoprotein [1,2].
This molecular mechanism explains why the test can have direct clinical relevance: the variant changes the function of a transporter involved in drug distribution.
The clinical effect is dose- and drug-dependent, and heterozygous dogs can have an intermediate phenotype for some P-glycoprotein substrates. In practical genetic reporting, the three possible genotypes are:
N/N – no copy of the tested ABCB1 deletion;
N/MDR1 – one copy of the deletion;
MDR1/MDR1 – two copies of the deletion.
Dogs with two copies generally have the greatest risk of clinically important drug sensitivity, while heterozygous dogs may also require additional caution depending on the drug and dose.
The variant is strongly associated with the Collie lineage and related herding breeds. It has been identified in populations of Collies, Australian Shepherds, Shetland Sheepdogs and several other related breeds and crosses. A large breed-distribution study showed that the mutation is not confined to one single breed and reflects shared ancestry within this lineage [2].
An MDR1-positive dog can be completely healthy and show no clinical signs whatsoever until exposed to a relevant drug. This is why the test is useful even in a young, apparently healthy dog.
When neurotoxicity occurs, the clinical picture depends on the drug and dose. Reported signs with macrocyclic lactone toxicity have included:
hypersalivation;
vomiting;
disorientation or altered mental status;
ataxia and loss of coordination;
tremors;
marked depression;
mydriasis;
recumbency;
seizure-like activity;
severe cases progressing to non-responsiveness or coma.
Experimental work in Collies demonstrated a very wide difference in ivermectin sensitivity between individuals, with severe neurological toxicity occurring in susceptible dogs at doses tolerated by others [3].
ABCB1/P-glycoprotein interacts with multiple veterinary drugs. The clinically important point is not to use a DNA result as a do-it-yourself medication list. Drug risk depends on the compound, formulation, dose, route, concurrent medications and the dog's genotype. The MDR1 result should therefore be recorded permanently in the dog's medical history and communicated to the treating veterinarian before prescribing potentially relevant drugs.
The genetic test establishes the ABCB1 genotype, but a dog presenting with neurological toxicity still requires clinical evaluation. Other intoxications and neurological diseases can produce similar signs. Genetic testing is most useful preventively before a problem occurs.
There is no treatment that can change the MDR1 genotype. The most important management is prevention of inappropriate drug exposure and genotype-aware prescribing.
If drug toxicity occurs, treatment is directed at the intoxication and can require intensive supportive care, fluid therapy and neurological, respiratory and cardiovascular monitoring depending on severity. In the original clinical observations of ivermectin-sensitive Collies, severely affected dogs recovered with supportive care, although toxicity can be life-threatening [3].
Because the variant is inherited, the genotype of the mating partner determines the expected genotypes of the offspring. A heterozygous dog can transmit the MDR1 allele to approximately half of its offspring. A homozygous variant dog transmits the variant to every offspring.
Genetic selection does not necessarily require removing every carrier from breeding immediately, particularly in breeds where maintaining genetic diversity is important. The practical objective is to know the genotype and plan matings accordingly.
If you are searching specifically for an MDR1 dog test, there is usually little reason to stop after one result. MDR1 is included in our breed-specific canine genetic panels together with DM, prcd-PRA, CDPA/CDDY and additional genetic tests specific to the breed. The complete breed-specific panel costs less than €100.
That means the same DNA sample can provide information about drug sensitivity and multiple inherited disorders relevant to future health and breeding.
Degenerative Myelopathy (DM) is a progressive neurodegenerative disease of the spinal cord. It is one of the most frequently requested canine DNA tests because affected dogs may appear completely normal for many years before developing a slowly progressive loss of hind-limb function.
The best-characterised genetic risk factor for canine DM is found in SOD1, the gene encoding superoxide dismutase 1. This enzyme participates in cellular defence against oxidative stress. Mutant SOD1 is also important in some forms of human amyotrophic lateral sclerosis, which is one reason canine DM has been extensively investigated as a comparative model of neurodegeneration.
The common canine DM-associated variant is SOD1:c.118G>A, which changes glutamic acid to lysine at amino-acid position 40, commonly abbreviated p.E40K. The original genome-wide association study identified homozygosity for this allele as strongly associated with DM in several breeds [4].
This is one of the most important points when interpreting a DM test.
The common SOD1 variant behaves as an autosomal recessive risk allele, but with incomplete penetrance. Therefore:
N/N – two wild-type alleles; the tested SOD1 risk variant is absent;
N/DM – heterozygous carrier;
DM/DM – homozygous for the risk allele and genetically at increased risk.
However, DM/DM is not the same as a clinical diagnosis of degenerative myelopathy. Some homozygous dogs may never develop clinical disease during their lifetime, while a dog with neurological signs still requires evaluation for other spinal and neurological disorders.
DM is classically a late-onset disease. In the landmark genetic study, initial signs generally appeared in older dogs and consisted of upper motor neuron dysfunction in the pelvic limbs [4].
Early signs can include:
subtle hind-limb incoordination;
proprioceptive ataxia;
scuffing or dragging of the rear paws;
asymmetric wear of the nails;
difficulty rising;
crossing of the hind limbs while walking;
progressive hind-limb weakness.
As the disease progresses, the dog can develop:
increasing paraparesis;
loss of independent ambulation;
paraplegia;
lower motor neuron signs and muscle atrophy at later stages;
eventual involvement of the thoracic limbs;
in very advanced disease, broader neuromuscular and respiratory compromise can occur.
Pain is not typically the defining feature of DM, which is clinically useful because painful spinal disease may suggest an alternative or concurrent diagnosis.
A DNA test identifies genetic susceptibility. It does not prove that neurological signs are caused by DM.
Ante-mortem diagnosis is therefore based on the dog's age, history, neurological examination, compatible SOD1 genotype and crucially - exclusion of other causes of progressive myelopathy.
Depending on the patient, this may involve blood testing and advanced spinal imaging such as MRI to exclude compressive intervertebral disc disease, neoplasia, inflammatory disease and other structural causes.
The distinction is essential for responsible reporting: genotype is a risk result; clinical DM is a neurological diagnosis.
There is currently no established curative treatment that reverses the underlying neurodegeneration. Management is aimed at preserving mobility, function and quality of life for as long as possible.
Supportive management can include:
structured physiotherapy and rehabilitation;
controlled exercise appropriate to neurological status;
maintenance of healthy body condition;
non-slip flooring and environmental adaptations;
harnesses and mobility aids as weakness progresses;
prevention and treatment of secondary complications associated with reduced mobility.
A clinical study of dogs with suspected DM found substantially longer survival in dogs receiving intensive controlled physiotherapy compared with dogs receiving moderate or no physiotherapy, supporting rehabilitation as an important component of management [5]. Experimental regenerative approaches continue to be investigated, but they should not be presented as established curative therapy.
Because DM is a recessive risk condition, mating strategy matters.
For the tested SOD1 variant:
N/N × N/N → puppies are not expected to inherit the tested risk allele;
N/N × N/DM → approximately 50% N/N and 50% carriers; no DM/DM puppies expected;
N/DM × N/DM → approximately 25% N/N, 50% carriers and 25% DM/DM;
DM/DM × N/N → all puppies are expected to be carriers, not DM/DM.
This is why genetic testing can be used to reduce production of high-risk homozygous dogs without automatically eliminating every carrier from a breeding population.
For a breeding dog, this provides a more useful genetic picture than knowing the SOD1 genotype alone.
Progressive Retinal Atrophy (PRA) is a collective clinical term for a genetically heterogeneous group of inherited retinal degenerations. In other words, there is no single universal “PRA gene”. Different breeds can develop clinically similar progressive retinal degeneration because of variants in different genes.
One of the most widespread and best-characterised forms is progressive rod-cone degeneration (prcd-PRA).
The PRCD gene encodes a small protein located in photoreceptor outer segment discs. The protein is important for normal photoreceptor maintenance. Experimental work has shown that the disease-associated amino-acid change interferes with normal PRCD localisation and stability in photoreceptor cells [6,7].
The classic canine prcd-PRA mutation is PRCD:c.5G>A, a single nucleotide substitution that changes the second amino acid from cysteine to tyrosine: p.(Cys2Tyr), also written C2Y.
The mutation was identified through comparison of affected and normal dogs and showed concordance with prcd disease across multiple breeds [6]. It is a founder mutation that has subsequently been detected in a large number of dog breeds.
prcd-PRA is inherited as an autosomal recessive disease.
Typical results are:
N/N – clear for the tested prcd-PRA variant;
N/prcd – carrier;
prcd/prcd – genetically affected for prcd-PRA.
A carrier generally does not develop prcd-PRA because of this recessive variant but can transmit it to offspring.
The retina contains two major photoreceptor types: rods, which are particularly important for vision in dim light, and cones, which contribute strongly to daylight and colour vision.
In prcd-PRA, rod dysfunction and degeneration predominate early, followed later by progressive cone involvement. Recent longitudinal structural and functional work in PRCD-mutant dogs confirms a rod-dominant degeneration with progressive loss of the outer retina [8].
This explains the characteristic sequence of clinical signs.
The exact age of onset varies by breed and individual, but prcd-PRA is generally considered a progressive, often middle to late onset retinal disease.
Owners may first notice:
difficulty seeing in dim light;
reluctance to enter dark rooms or go outside at night;
bumping into objects in low-light conditions;
increased caution on stairs or unfamiliar terrain;
reduced confidence when lighting changes suddenly.
As cone function becomes affected, vision deteriorates in daylight as well. Advanced disease can progress to severe bilateral visual impairment or blindness.
Ophthalmic findings in PRA can include:
increased tapetal reflectivity;
attenuation of retinal blood vessels;
progressive retinal thinning and degeneration;
optic nerve changes in advanced disease;
secondary cataract formation in some affected dogs.
In a study of English Cocker Spaniels homozygous for the PRCD variant, clinical visual impairment was observed in the majority of genetically affected dogs that underwent ophthalmic examination, illustrating the clinical relevance of the genotype while also showing that age and disease stage influence the phenotype [9].
Genetic testing is particularly valuable because it can identify an affected genotype before obvious visual impairment develops.
When a dog already has visual signs, clinical evaluation may include:
complete ophthalmic examination;
fundoscopy;
electroretinography (ERG) to assess retinal function;
in specialist settings, optical coherence tomography (OCT) to evaluate retinal structure.
The DNA test and the ophthalmic examination answer different questions. DNA establishes whether the tested pathogenic variant is present; ophthalmology establishes whether retinal disease is clinically present and how advanced it is.
There is currently no routine curative treatment that restores photoreceptors lost through prcd-PRA. Molecular and gene-therapy approaches for inherited retinal diseases are an active research field, including successful experimental gene therapy in other canine inherited retinal disorders, but these approaches should not be confused with an established clinical treatment for a pet dog with prcd-PRA.
Management of an affected dog therefore focuses on:
veterinary ophthalmic monitoring;
maintaining a predictable home environment;
avoiding unnecessary rearrangement of furniture;
using lighting strategically as night vision deteriorates;
securing stairs, balconies, pools and other hazards;
using voice cues and environmental consistency to support a visually impaired dog.
Many dogs adapt surprisingly well to gradual vision loss because smell, hearing and spatial memory remain intact.
Because prcd-PRA is autosomal recessive:
N/N × N/N → all puppies expected to be clear;
N/N × N/prcd → approximately 50% clear and 50% carriers; no affected puppies expected;
N/prcd × N/prcd → approximately 25% clear, 50% carriers and 25% genetically affected;
prcd/prcd × N/N → all puppies expected to be carriers.
For breeding, the major advantage of DNA testing is that carriers can be identified even though they are clinically normal.
No. A dog can be clear for prcd-PRA and still be susceptible to a different inherited retinal disease caused by another gene. This is precisely why testing based on the breed is superior to assuming that a single generic PRA test covers every retinal condition.
Where a breed has additional known retinal variants, those breed-specific risks can be addressed within the broader panel rather than treating “PRA” as one universal mutation.
The IVDD genetic test is probably the most commonly misunderstood test in this group because it involves two different FGF4 retrogene insertions that are often reported together: CDPA and CDDY.
They are not the same variant and they do not have the same clinical significance.
FGF4 (fibroblast growth factor 4) normally has important roles in growth and development. In dogs, additional retrotransposed copies of FGF4 have become inserted into other chromosomes during canine evolution.
Two of these FGF4 retrogenes are particularly important:
| Test | Genetic event | Chromosome | Main association |
|---|---|---|---|
| CDPA | 18-FGF4 retrogene insertion | CFA18 | Disproportionately short limbs / chondrodysplasia |
| CDDY | 12-FGF4 retrogene insertion | CFA12 | Shortened limbs, premature intervertebral disc degeneration and increased IVDD susceptibility |
The distinction matters because a dog can have the short-legged phenotype associated with CDPA without carrying the CFA12 CDDY variant that has the much stronger association with intervertebral disc disease.
The FGF4 retrocopy on chromosome 18 is strongly associated with disproportionate dwarfism / shortened long bones in several breeds. It contributes to the characteristic conformation of some short-legged breeds.
CDPA should therefore not automatically be described to an owner as “the IVDD mutation”. Its principal recognised effect is on skeletal morphology.
This distinction is particularly relevant in breed-specific interpretation. In a breed where short limbs are part of normal breed type, the presence of CDPA can have a completely different breeding significance from the presence of CDDY.
The FGF4 retrogene on chromosome 12 is associated with chondrodystrophy and premature degeneration of intervertebral discs. Brown and colleagues identified a very strong association between the CFA12 FGF4 retrogene and IVDD across breeds [10].
A later study of hundreds of dogs undergoing surgery for IVDD found that the 12-FGF4 retrogene was associated with younger age at first surgery, greater disc calcification and increased risk of disc herniation, whereas the CFA18 retrogene did not show the same strong relationship with disc disease [11].
This is why an accurate report must keep CDPA (CFA18) and CDDY (CFA12) separate.
In chondrodystrophic disc degeneration, the nucleus pulposus undergoes premature degenerative change, losing normal hydration and becoming more cartilaginous and, in some dogs, mineralised. Degenerated disc material can then herniate into the vertebral canal and compress or injure the spinal cord or nerve roots.
Importantly, having the CDDY genotype is not the same as currently having a herniated disc. The DNA result identifies inherited susceptibility. Whether an individual dog develops a clinically significant disc extrusion depends on additional genetic, anatomical and environmental factors.
Clinical signs depend on the location and severity of disc herniation. They can range from pain alone to severe paralysis.
Possible signs include:
neck or back pain;
reluctance to jump, climb stairs or move normally;
a hunched or guarded posture;
trembling or vocalisation associated with pain;
ataxia and an unsteady gait;
weakness of one or more limbs;
knuckling or proprioceptive deficits;
inability to walk;
paralysis;
urinary dysfunction or incontinence in severe neurological cases.
Thoracolumbar disc disease is a well-recognised cause of back pain, pelvic-limb paresis or paralysis and urinary dysfunction in dogs [12].
A genetic test cannot diagnose an acute disc herniation.
If a dog develops compatible neurological signs, diagnosis requires veterinary neurological assessment and, where indicated, advanced imaging such as MRI or CT. Imaging determines where the lesion is, what type of disc disease is present and how severely neural tissue is compressed.
The roles are therefore different:
CDDY/CDPA DNA testing = inherited risk and breeding information;
neurological examination + imaging = diagnosis of the individual clinical episode.
There is no treatment that removes the inherited FGF4 retrogene from the dog. Treatment is necessary only if the dog develops clinical IVDD or another associated problem.
Management of clinical IVDD depends on neurological severity and imaging findings and may include:
strict activity restriction in appropriately selected mild cases;
veterinary analgesia and medical management;
rehabilitation after the acute phase where appropriate;
surgical decompression in dogs with significant spinal cord compression or neurological deficits.
Clinical studies demonstrate that both medical and surgical management are used in canine intervertebral disc disease, with case selection strongly influenced by neurological severity; in one retrospective study of thoracolumbar disc protrusion, sustained successful outcomes were more common in surgically treated dogs, although the surgical group also contained more neurologically affected patients [13].
A dog that is acutely unable to walk, rapidly deteriorating or losing pain perception should be considered a neurological emergency rather than managed on the basis of its genetic test result.
For the CFA12 retrogene, one copy is clinically relevant because the association with IVDD behaves substantially in a dominant manner. Therefore, breeding two CDDY-positive dogs can increase the number of offspring carrying the risk allele, while an N/N parent cannot transmit CDDY.
At the same time, breeding policy should be breed-specific. In some populations, the CDDY allele is common and very aggressive elimination could reduce genetic diversity. Genetic results are most useful when combined with breed structure, family history, phenotype and the genotype of the intended mating partner.
CDPA is primarily a morphology-associated variant. A CDPA/CDPA result in a characteristically short-legged breed should not automatically be described as equivalent to being homozygous for CDDY/IVDD risk. This is exactly why laboratories should report the two FGF4 insertions separately.
The four tests discussed above answer four very different biological questions:
MDR1 / ABCB1: can this dog's genotype increase susceptibility to adverse effects from certain drugs?
DM / SOD1: does the dog carry a major genetic risk factor for late-onset degenerative myelopathy?
prcd-PRA / PRCD: does the dog carry the common recessive variant responsible for progressive rod-cone degeneration?
CDPA/CDDY / FGF4: does the dog carry either of the two major FGF4 retrogene insertions affecting limb phenotype and, for CFA12, IVDD susceptibility?
Ordering each one separately still leaves another problem: your breed may have additional inherited disorders that are more specific to that breed.
That is why Animalabs uses a broader breed-specific approach. Our breed-specific canine genetic panels include the core tests discussed in this article — MDR1, DM, prcd-PRA and CDPA/CDDY — and add further genetic tests selected for the breed.
The result is:
one DNA sample;
one laboratory submission;
the major widely requested canine genetic tests;
additional breed-specific disease variants;
one integrated genetic report;
a complete breed-specific panel for less than €100.
For a breeder, the meaningful question is therefore not simply “Should I order MDR1 or DM?” but rather “What inherited risks should I know before choosing a mating partner?”
DNA is stable throughout life, which makes pre-breeding genetic testing especially useful. Once a dog's genotype is known, that information can be used when selecting mating partners and evaluating future generations.
For autosomal recessive diseases, a carrier can often be bred responsibly to a genetically clear partner without producing genetically affected puppies for that specific condition. For dominant or risk-associated variants, breeding decisions require a different interpretation.
This is another reason why a panel accompanied by clear laboratory interpretation is more valuable than simply receiving a list of mutation names.
At Animalabs, the objective is not to label every positive genetic result as a reason to exclude a dog from breeding. The objective is to provide information that allows breeders and veterinarians to make informed decisions while considering both inherited disease risk and the genetic diversity of the breed.
If you already know exactly which single mutation you need, an individual genetic test may be sufficient.
But if your dog is being tested before breeding, the more useful question is usually:
Which inherited conditions are relevant to my breed?
That is why we recommend starting with the dog's breed rather than starting with the name of one mutation.
An Animalabs breed-specific panel can combine the major genetic tests relevant to that breed in one analysis, including highly searched tests such as MDR1, DM, PRA and CDDY/IVDD where appropriate, together with additional breed-specific genetic conditions.
Total panel price: less than €100.
MDR1/ABCB1 is included as part of the Animalabs breed-specific genetic panel together with additional breed-relevant DNA tests.
Usually not if the breed has other known inherited conditions. DM is only one genetic risk. A breed-specific panel provides a broader picture from the same DNA sample.
No. PRA is genetically heterogeneous. A clear result applies to the specific tested variant. Different breeds can require different retinal DNA tests.
No. CDPA and CDDY are separate FGF4 retrogene insertions on different chromosomes. CDDY on CFA12 is associated with premature intervertebral disc degeneration and increased susceptibility to IVDD, while CDPA on CFA18 is primarily associated with shortened limb phenotype.
For many autosomal recessive disorders, a carrier may be bred to a genetically clear partner without producing affected puppies for that specific mutation. Breeding decisions should consider the inheritance pattern, the partner's genotype and the genetic diversity of the breed.
Animalabs breed-specific canine genetic panels are priced below €100 and combine multiple relevant genetic tests rather than requiring the breeder to purchase each common mutation individually.
Explore InovaGen breed-specific dog DNA panels or contact our laboratory and tell us your dog's breed. We will help you identify the appropriate genetic panel.
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Spencer WJ, Pearring JN, Salinas RY, et al. Progressive Rod-Cone Degeneration (PRCD) Protein Requires N-Terminal S-Acylation and Rhodopsin Binding for Photoreceptor Outer Segment Localization and Maintaining Intracellular Stability. Molecular Biology of the Cell. 2016;27. PMID: 27509380.
Dufour VL, Sato Y, Sumaroka A, et al. PRCD-associated retinitis pigmentosa in dogs and humans. Experimental Eye Research. 2026;269:111045. DOI: 10.1016/j.exer.2026.111045.
Santana E, et al. Allele Frequency of the c.5G>A Mutation in the PRCD Gene Responsible for Progressive Retinal Atrophy in English Cocker Spaniel Dogs. Animals. 2019. PMCID: PMC6826964.
Brown EA, Dickinson PJ, Mansour T, et al. FGF4 retrogene on CFA12 is responsible for chondrodystrophy and intervertebral disc disease in dogs. Proceedings of the National Academy of Sciences USA. 2017;114(43):11476–11481. DOI: 10.1073/pnas.1709082114.
Batcher K, Dickinson P, Giuffrida M, et al. Phenotypic Effects of FGF4 Retrogenes on Intervertebral Disc Disease in Dogs. Genes. 2019;10(6):435. DOI: 10.3390/genes10060435.
Freeman P, Jeffery ND. Re-opening the window on fenestration as a treatment for acute thoracolumbar intervertebral disc herniation in dogs. Journal of Small Animal Practice. 2017. PMID: 28276121.
Crawford AH, De Decker S. Clinical presentation and outcome of dogs treated medically or surgically for thoracolumbar intervertebral disc protrusion. Veterinary Record. 2017;180(23):569. DOI: 10.1136/vr.103871.
Veterinary genetics disclaimer: A DNA result applies to the specific genetic variant tested. Genetic testing does not replace clinical veterinary examination or other breed-recommended health screening. Results should be interpreted according to the inheritance pattern, breed and intended breeding combination.