Neurons acetylate their way to migration. (21st October 2016)

• Record Type: Journal Article
• Authors: Borrie, Sarah Catherine; Bagni, Claudia
• Is Part Of: EMBO reports. Volume 17:Number 12(2016:Dec.)
• Page Start: 1674
• Page End: 1676
• Publication Date: 2016-10-21
• Subjects: Molecular biology -- Periodicals; Molecular Biology -- Periodicals; Molecular biology; Periodicals; 572.8
• DOI: 10.15252/embr.201643427
• Languages: English
• ISSNs: 1469-221X

Abstract

Abstract : The centrosome is crucial for neuronal migration and polarisation, processes that are disrupted in a number of neurodevelopmental disorders including schizophrenia. Mutation of DISC1, associated with increased risk of schizophrenia and psychiatric illness, has been shown to affect the centrosome, but the mechanisms involved have not been elucidated. In this issue of EMBO Reports, Fukuda and colleagues demonstrate that a DISC1‐interacting protein, CAMDI, suppresses the activity of the histone deacetylase HDAC6, thereby promoting centrosome stability and consequently neuronal migration 1 . Loss of CAMDI leads to cortical migration defects and behavioural phenotypes that model autism spectrum disorders and which can be rescued by inhibition of HDAC6. The study provides novel mechanistic insight into centrosome regulation in neurodevelopment. Abstract : A study in this issue shows that CAMDI loss leads to cellular and behavioural phenotypes that model autism spectrum disorders and which can be ameliorated by HDAC6 inhibition.