{"id":493,"date":"2025-10-08T17:18:00","date_gmt":"2025-10-08T15:18:00","guid":{"rendered":"https:\/\/dev.genocan.eu\/2025\/10\/08\/genetika-rhodeskeho-ridgebacka-vysledky-400-geneticky-vysetrenych-psu\/"},"modified":"2026-05-23T13:37:14","modified_gmt":"2026-05-23T11:37:14","slug":"genetics-of-the-rhodesian-ridgeback-population-findings-from-400-tested-dogs","status":"publish","type":"post","link":"https:\/\/dev.genocan.eu\/en\/2025\/10\/08\/genetics-of-the-rhodesian-ridgeback-population-findings-from-400-tested-dogs\/","title":{"rendered":"Genetics of the Rhodesian Ridgeback: Population findings from 400 tested dogs"},"content":{"rendered":"

Dear breeders, we would like to share with you data from genetic testing. We believe that this data will be a valuable aid and will facilitate your understanding of the genetics of Rhodesian Ridgebacks.<\/p>\n

Below is a summary table covering all genetic diseases and traits assessed in the RR PANEL + RRIVA testing (Rhodesian Ridgeback | GenoCan.eu<\/span>). The table reflects results from 400 Rhodesian Ridgebacks<\/strong> collected across Europe, with most samples coming from the Czech Republic, Slovakia, Germany, the Netherlands, Denmark, France, Sweden, Norway, Austria, and the United Kingdom. Below the table you will find more detailed and commented findings of individual diseases\/traits.<\/p>\n\n\n\n\n\n\n\n\n\n\n\n\n\n
Trait \/ Disease<\/th>\nWild-type<\/th>\nCarrier<\/th>\nAt risk<\/th>\n<\/tr>\n<\/thead>\n
Ridge predisposition (RIDGE)<\/strong><\/td>\nR\/R:<\/strong> 50% (200)<\/td>\nR\/r:<\/strong> 50% (200)<\/td>\nr\/r:<\/strong> 0% (0)<\/td>\n<\/tr>\n
Juvenile Myoclonic Epilepsy (JME)<\/strong><\/td>\nN\/N:<\/strong> 94% (376)<\/td>\nP\/N:<\/strong> 6% (24)<\/td>\nP\/P:<\/strong> 0% (0)<\/td>\n<\/tr>\n
Malignant Hyperthermia (MH)<\/strong><\/td>\nN\/N:<\/strong> 100% (400)<\/td>\nP\/N:<\/strong> 0% (0)<\/td>\nP\/P:<\/strong> 0% (0)<\/td>\n<\/tr>\n
Degenerative Myelopathy (DM)<\/strong><\/td>\nN\/N:<\/strong> 91% (364)<\/td>\nP\/N:<\/strong> 9% (36)<\/td>\nP\/P:<\/strong> 0% (0)<\/td>\n<\/tr>\n
D-Locus (dilute) (DLOK)<\/strong><\/td>\nD\/D:<\/strong> 93% (372)<\/td>\nD\/d1:<\/strong> 7% (28)<\/td>\nd1\/d1:<\/strong> 0% (0)<\/td>\n<\/tr>\n
B-Locus (brown) (BLOK)<\/strong><\/td>\nB\/B:<\/strong> 71% (284)<\/td>\nB\/b:<\/strong> 25% (100)<\/td>\nb\/b:<\/strong> 4% (16)<\/td>\n<\/tr>\n
Hemophilia B (HEMB)<\/strong><\/td>\nN\/N:<\/strong> 100% (400)<\/td>\nP\/N:<\/strong> 0% (0)<\/td>\nP\/P:<\/strong> 0% (0)<\/td>\n<\/tr>\n
Early Onset Adult Deafness (EOAD)<\/strong><\/td>\nN\/N:<\/strong> 96% (384)<\/td>\nP\/N:<\/strong> 4% (16)<\/td>\nP\/P:<\/strong> 0% (0)<\/td>\n<\/tr>\n
Inherited Ventricular Arrhythmia (RRIVA)<\/strong><\/td>\nN\/N:<\/strong> 60% (239)<\/td>\nP\/N:<\/strong> 38% (151)<\/td>\nP\/P:<\/strong> 2.5% (10)<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

Notes:<\/strong> N = normal\/wild-type allele; P = risk variant allele. RIDGE: R confers ridge predisposition (R\/R or R\/r), r\/r lacks the ridge. DLOK\/BLOK are coat-color loci (not disease).<\/p>\n

Ridge predisposition (RIDGE)<\/h2>\n

Based on testing of 400 Rhodesian Ridgebacks for ridge gene, we can conclude that there is equal number of R\/R (Ridge \/ Ridge) and R\/r (Ridge \/ ridgeless)<\/strong> genotypes in Rhodesian ridgeback population. R\/R dogs typically do not produce ridgeless dogs, on the other hand R\/r are at risk of producing numerous ridgeless dogs when mated with another R\/r. Based on our laboratory data, R\/R dogs are at approximately 2x higher risk<\/strong> of Dermoid Sinus (DS) or ridge irregularities (multicrowns) compared to R\/r. That’s very likely why R\/r dogs are preferable genotypes and that explains relatively high frequency of this genotype in Rhodesian ridgeback population despite the fact they are at risk of producing ridgeless.<\/p>\n

Juvenile Myoclonic Epilepsy (JME)<\/h2>\n

JME is an inherited epilepsy of Rhodesian Ridgebacks characterized by myoclonic (jerk-like) seizures beginning in youth. In our cohort of 400 dogs, ~6% were carriers<\/strong> of the JME variant.<\/p>\n

Inheritance & risk (autosomal recessive):<\/strong><\/p>\n

    \n
  • Carrier \u00d7 Carrier (P\/N \u00d7 P\/N):<\/strong> 25% affected (P\/P)<\/strong>, 50% carriers (P\/N)<\/strong>, 25% clear (N\/N)<\/strong>.<\/li>\n
  • Carrier \u00d7 Clear (P\/N \u00d7 N\/N):<\/strong> 0% affected; 50% carriers, 50% clear.<\/li>\n
  • Clear \u00d7 Clear (N\/N \u00d7 N\/N):<\/strong> 100% clear.<\/li>\n<\/ul>\n

    Breeding guidance:<\/strong>
    Avoid P\/N \u00d7 P\/N<\/strong> matings to eliminate the 25% risk of affected puppies. Pairing carriers with genetically clear mates prevents affected offspring while maintaining genetic diversity.<\/p>\n

    Malignant Hyperthermia (MH)<\/h2>\n

    MH is an autosomal dominant<\/strong> condition: dogs carrying the pathogenic variant (P\/N<\/strong>) are at risk<\/strong> for malignant hyperthermia\u2014an anesthetic-triggered crisis with rapid hyperthermia and severe muscle rigidity. In our cohort of 400 Rhodesian Ridgebacks, no MH-positive dogs were detected<\/strong> (100% N\/N<\/strong>), suggesting very low or zero prevalence<\/strong> in this population.<\/p>\n

    Degenerative myelopathy (DM)<\/h2>\n

    DM is a late-onset, progressive neurodegenerative disease. Early signs can include wobbliness\/loss of balance, a limp tail, dragging of the hind feet, urinary\/fecal incontinence, and, over time, hind-limb paralysis. Genetic status informs about risk, but clinical evaluation<\/strong> is still essential.<\/p>\n

    D-Locus (dilute) \u2014 DLOK<\/h2>\n

    The D-locus controls pigment dilution<\/strong>. The tested variant (d1<\/strong>) reduces pigment intensity. In Rhodesian Ridgebacks<\/strong> a dilution lightens the typical red-wheaten coat to a cream\/blue<\/strong> shade.<\/p>\n

    Our cohort (n = 400)<\/strong><\/p>\n

      \n
    • D\/D:<\/strong> 93% (372)<\/li>\n
    • D\/d1 (carriers):<\/strong> 7% (28)<\/strong><\/li>\n
    • d1\/d1:<\/strong> 0% (0)<\/li>\n<\/ul>\n

      Notes:<\/em> Dilution primarily affects pigment and is not a disease. Some breeds associate dilute color with coat\/skin issues (e.g., color dilution alopecia), but prevalence varies by breed.<\/p>\n

      B-Locus (brown) \u2014 BLOK<\/h2>\n

      The B-locus controls brown vs. black eumelanin. There are three variants tested (each predisposing to brown coloration) and the inheritance is autosomal recessive<\/strong>.<\/p>\n

      Phenotype in Rhodesian Ridgebacks<\/strong><\/p>\n

        \n
      • b\/b (brown\/liver):<\/strong> brown (“liver”) nose, lips, eye rims, and claws; coat pigment shifts toward brown tones.<\/li>\n
      • B\/B or B\/b:<\/strong> black pigment on nose\/skin (non-brown). Carriers (B\/b<\/strong>) look normal black.<\/li>\n<\/ul>\n

        Our cohort (n = 400)<\/strong><\/p>\n

          \n
        • B\/B:<\/strong> 71%<\/strong> (284)<\/li>\n
        • B\/b (carriers):<\/strong> 25%<\/strong> (100)<\/li>\n
        • b\/b (brown\/liver):<\/strong> 4%<\/strong> (16)<\/li>\n<\/ul>\n

          Breeding guidance<\/strong><\/p>\n

            \n
          • Carrier \u00d7 Carrier (B\/b \u00d7 B\/b):<\/strong> 25% b\/b (brown), 50% carriers, 25% B\/B<\/li>\n
          • Carrier \u00d7 Clear (B\/b \u00d7 B\/B):<\/strong> 0% b\/b; 50% carriers, 50% B\/B<\/li>\n
          • Clear \u00d7 Clear (B\/B \u00d7 B\/B):<\/strong> 100% B\/B<\/li>\n<\/ul>\n

            Hemophilia B (HEMB)<\/h2>\n

            Hemophilia B is an X-linked<\/strong> hereditary bleeding disorder caused by deficiency or dysfunction of Factor IX (F9)<\/strong>. Affected dogs form clots poorly, so even minor trauma, surgery, or spontaneous internal bleeding can be life-threatening.<\/p>\n

            Who is affected?<\/strong>
            Because HEMB is X-linked, males (XY)<\/strong> with the variant are typically affected, while females (XX)<\/strong> are usually carriers.<\/p>\n

            In our cohort, no dogs tested were affected or identified as carriers for Hemophilia B<\/strong> (N\/N: 400; P\/N: 0; P\/P: 0). Based on breeders data there are no carriers also for Hemophilia A<\/strong>. These results suggest that both Hemophilia B and A are extremely rare in RR population<\/strong>.<\/p>\n

            Early Onset Adult Deafness (EOAD)<\/h2>\n

            EOAD is an inherited condition in which affected Rhodesian Ridgebacks progress to deafness within ~1\u20132 years of age<\/strong>. Puppies are typically born hearing; loss develops early in life.<\/p>\n

            Genetics<\/strong><\/p>\n

              \n
            • Autosomal recessive<\/strong> inheritance.<\/li>\n
            • An affected dog (P\/P<\/strong>) is produced when both parents are carriers<\/strong> (P\/N \u00d7 P\/N<\/strong>).<\/li>\n
            • Carriers (P\/N)<\/strong> have normal hearing and do not<\/strong> develop EOAD.<\/li>\n<\/ul>\n

              Our cohort (n = 400)<\/strong><\/p>\n

                \n
              • Clear: 96% (384\/400)<\/strong><\/li>\n
              • Carriers:<\/strong> ~4%<\/strong> (16\/400)<\/li>\n
              • Affected (P\/P):<\/strong> 0% detected<\/strong><\/li>\n<\/ul>\n

                Pair genetic testing with BAER hearing assessments<\/strong> when EOAD is a concern, and note results in breeding and veterinary records.<\/p>\n

                Inherited Ventricular Arrhythmia (RRIVA)<\/h2>\n

                An initial research report led by Dr. Kathryn Meurs<\/strong> described a genetic variant associated with Inherited Ventricular Arrhythmia<\/strong> in Rhodesian Ridgebacks (RR). However, follow-up testing in 400 RR dogs<\/strong> indicates that the variant is too common<\/strong> in the breed and does not track reliably<\/strong> with the presence or absence of ventricular arrhythmias leading to sudden death. In other words, the variant shows poor predictive value<\/strong> for disease in this population. Although a candidate variant was initially reported, current evidence suggests it does not explain ventricular arrhythmia risk<\/strong> leading to sudden death in the broader RR population; therefore, routine genetic testing for this variant is unlikely to be beneficial<\/strong>. The article about RRIVA is available here: Does it make sense to test for Inherited Ventricular Arrhythmia (RR IVA) in Rhodesian Ridgebacks? | GenoCan.eu<\/span><\/p>\n\n\n\n\n\n
                N\/N \u2013 (standard variant)<\/td>\nn=239 (60%)<\/td>\n<\/tr>\n
                P\/N \u2013 (alternative variant carrier)<\/td>\nn=151 (38%)<\/td>\n<\/tr>\n
                P\/P \u2013 (alternative variant homozygote)<\/td>\nn=10 (2.5%)<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

                What this means in practice<\/strong><\/p>\n

                  \n
                • The currently available RRIVA genetic test has very low clinical utility<\/strong> in Rhodesian Ridgebacks.<\/li>\n
                • A negative<\/strong> result does not<\/strong> rule out ventricular arrhythmias, and a positive<\/strong> result does not<\/strong> confirm disease.<\/li>\n
                • Decisions about breeding or clinical management should not<\/strong> be based on this variant alone.<\/li>\n<\/ul>\n","protected":false},"excerpt":{"rendered":"

                  Dear breeders, we would like to share with you data from genetic testing. We believe that this data will be a valuable aid and will facilitate your understanding of the genetics of Rhodesian Ridgebacks. Below is a summary table covering all genetic diseases and traits assessed in the RR PANEL + RRIVA testing (Rhodesian Ridgeback […]<\/p>\n","protected":false},"author":1,"featured_media":494,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"footnotes":""},"categories":[134],"tags":[],"kat":[],"class_list":["post-493","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-novinka"],"acf":[],"_links":{"self":[{"href":"https:\/\/dev.genocan.eu\/en\/wp-json\/wp\/v2\/posts\/493","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/dev.genocan.eu\/en\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/dev.genocan.eu\/en\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/dev.genocan.eu\/en\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/dev.genocan.eu\/en\/wp-json\/wp\/v2\/comments?post=493"}],"version-history":[{"count":2,"href":"https:\/\/dev.genocan.eu\/en\/wp-json\/wp\/v2\/posts\/493\/revisions"}],"predecessor-version":[{"id":563,"href":"https:\/\/dev.genocan.eu\/en\/wp-json\/wp\/v2\/posts\/493\/revisions\/563"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/dev.genocan.eu\/en\/wp-json\/wp\/v2\/media\/494"}],"wp:attachment":[{"href":"https:\/\/dev.genocan.eu\/en\/wp-json\/wp\/v2\/media?parent=493"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/dev.genocan.eu\/en\/wp-json\/wp\/v2\/categories?post=493"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/dev.genocan.eu\/en\/wp-json\/wp\/v2\/tags?post=493"},{"taxonomy":"kat","embeddable":true,"href":"https:\/\/dev.genocan.eu\/en\/wp-json\/wp\/v2\/kat?post=493"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}