Histone deacetylation-dependent and -independent transcriptional dysregulation in early-onset polyglutamine disease

ABSTRACT: Transcriptional dysregulation is an important early feature of polyglutamine diseases. One of its proposed causes is defective neuronal histone acetylation, but important aspects of this hypothesis, such as the precise genomic topography of acetylation deficits and the relationship between transcriptional and acetylation alterations at the whole-genome level, remain unknown. The new techniques for the mapping of histone posttranslational modifications at genomic scale enable such global analyses and are challenging important assumptions concerning the role of specific histone modifications in gene expression. We examined here the genome-wide correlation of histone acetylation and gene expression defects in a mouse model of early-onset Huntington’s disease. Our analyses identified hundreds

ORGANISM(S): Mus musculus

SUBMITTER: Luis Valor 

PROVIDER: E-GEOD-44854 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress