E-GEOD-48962 - Transcription profiling by high throughput sequencing in wild type and R6/2 mutant mouse cortex and striatum at 8 and 12 weeks
Released on 18 July 2013, last updated on 12 May 2016
Transcriptional dysregulation is an early feature of Huntington's disease (HD). We observed gene-specific changes in H3K4me3 at transcriptionally repressed promoters in R6/2 mouse and human HD brain. Genome-wide analysis showed a novel chromatin signature for this mark. Reducing the levels of the H3K4 demethylase SMCX/Jarid1c in primary neurons reversed down-regulation of key neuronal genes caused by mutant Huntingtin (Htt) expression. Finally, reduction of SMCX/Jarid1c in primary neurons from BACHD mice or the single Jarid1 in a Drosophila HD model was protective. Therefore, targeting this epigenetic signature may be an effective strategy to ameliorate the consequences of HD. mRNA-seq in wild type and R6/2 cortex and striatum at 8 and 12 weeks.
RNA-seq of coding RNA
Christopher Ng <firstname.lastname@example.org>, Christopher W Ng, David Housman, Ernest Fraenkel, Leslie M Thompson, Malini Vashishtha, Theresa Gipson
Targeting H3K4 trimethylation in Huntington disease. Vashishtha M, Ng CW, Yildirim F, Gipson TA, Kratter IH, Bodai L, Song W, Lau A, Labadorf A, Vogel-Ciernia A, Troncosco J, Ross CA, Bates GP, Krainc D, Sadri-Vakili G, Finkbeiner S, Marsh JL, Housman DE, Fraenkel E, Thompson LM. , Europe PMC 23872847