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Basenji pack: progressive retinal atrophy (Bas-PRA1) + pyruvate kinase deficiency (PK) + Fanconi syndrome

General · Dog

Genetic panel for the Basenji that groups three classic recessive hereditary conditions of the breed: Bas-PRA1 progressive retinal atrophy (adult-onset form of PRA due to SAG), pyruvate kinase deficiency (PK, chronic haemolytic anaemia due to a defect in erythrocyte glycolysis) and Fanconi syndrome (proximal renal tubular dysfunction with glucosuria, aminoaciduria and metabolic acidosis). All three have a well-characterised molecular basis and a specific genetic test.
Inheritance patternAutosomal recessive for all three conditions
Gene / MutationSAG c.1216T>C p.(*405Rext*25) (Bas-PRA1; OMIA:001876-9615); PKLR 1 bp deletion, c.433del p.(P145Rfs*23) (Basenji PK; OMIA:000844-9615); FAN1 317 bp deletion in exon 14, c.2954_3090+181del p.(Leu985ValfsTer19) (Fanconi; OMIA:002683-9615).
PenetranceHigh penetrance in homozygotes for all three. In Fanconi, onset is variable and environmental factors (toxins) are postulated as modulators. Heterozygotes asymptomatic.
Codejbnk
Turnaround time15 days
Price110,73 €

Incidence

Basenji. PK deficiency and Fanconi syndrome are well characterised in the breed; carrier frequencies by country are not published systematically (limited data). Bas-PRA1 is relatively uncommon but should be screened for.

Breeder management

- Genotype breeding animals for SAG, PKLR and FAN1 before mating\n- Do not cross two carriers for the same variant\n- A carrier may be crossed with a clear animal and offspring intended for breeding must be tested\n- After a confirmed case, do not repeat the parental cross and communicate the status to the buyer\n- Adult-onset Fanconi makes genetic screening the only way to prevent transmission: animals that are clinically healthy at a young age may be carriers or even non-expressing homozygotes

Specialist notes

Bas-PRA1 must be distinguished from other PRAs of the Basenji: there is at least one other form not attributable to SAG. PK deficiency must be distinguished from other haemolytic anaemias (phosphofructokinase, pyrimidine 5'-nucleotidase). Basenji Fanconi must be distinguished from toxin-acquired Fanconi (gentamicin, tenofovir) and from diabetes mellitus (the Basenji with Fanconi is normoglycaemic with glucosuria). Management of Fanconi requires bicarbonate supplementation and analytical monitoring.

References

1. Goldstein O et al. 2013. A non-stop S-antigen gene mutation is associated with late onset hereditary retinal degeneration in dogs. Mol Vis. PMID: 24019744. 2. Whitney KM et al. 1994. The molecular basis of canine pyruvate kinase deficiency. Exp Hematol. PMID: 7520391. 3. Farias FHG et al. 2024. FAN1 deletion variant in Basenji dogs with Fanconi syndrome. Genes (Basel). PMID: 39596669. OMIA:001876-9615, OMIA:000844-9615, OMIA:002683-9615.

Tests included in this pack (3)

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