RARb and Huntington Disease

Our working hypothesis is that two genetic factors A (compromized Rarß expression in Rarß+/- mice) and B (mutant form of huntingtin; R6/1 Tg/0) can synergise in generating physiopathology of Huntington disease. To address this point we performed comparative transcritomics in the nucleus accumbens (NAc) for 4 experimental groups : 1) R6/1 Tg/0 ; Rarß+/-, (n=3); 2) R6/1 Tg/0 ; Rarß+/+, (n=3); 3) R6/1 0/0 ; Rarß+/-, (n=3); 4) R6/1 0/0 ; Rarß+/+ (n=2). Overall design: RNAs were extracted from 12 samples (as described in the summary) collected from 8-week-old mice to evaluate transcriptional changes associated with decreased Rarß signaling in the context of HD-causing mutation. Sample 10 (male 80, R6/1 0/0 ; Rarß+/+) did not pass the quality control and was excluded. Samples were sequenced according to the attached protocol