Polyglutamine-expanded ATXN7 alters a specific epigenetic signature underlying photoreceptor identity gene expression in SCA7 mouse retinopathy.
Fiche publication
Date publication
décembre 2022
Journal
Journal of biomedical science
Auteurs
Membres identifiés du Cancéropôle Est :
Mme MESSADDEQ Nadia
Tous les auteurs :
Niewiadomska-Cimicka A, Hache A, Le Gras S, Keime C, Ye T, Eisenmann A, Harichane I, Roux MJ, Messaddeq N, Clérin E, Léveillard T, Trottier Y
Lien Pubmed
Résumé
Spinocerebellar ataxia type 7 (SCA7) is a neurodegenerative disorder that primarily affects the cerebellum and retina. SCA7 is caused by a polyglutamine expansion in the ATXN7 protein, a subunit of the transcriptional coactivator SAGA that acetylates histone H3 to deposit narrow H3K9ac mark at DNA regulatory elements of active genes. Defective histone acetylation has been presented as a possible cause for gene deregulation in SCA7 mouse models. However, the topography of acetylation defects at the whole genome level and its relationship to changes in gene expression remain to be determined.
Mots clés
Epigenomics, Neuronal identity, Photoreceptor dystrophy, SAGA, Spinocerebellar ataxia type 7, Transcriptomics
Référence
J Biomed Sci. 2022 12 20;29(1):107