ChIP-Seq of H3K4 methylation in neurons isolated from E16.5 mouse embryonic cortices from WT and SMCX KO mice
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ABSTRACT: We conducted ChIP-Seq of H3K4 methylation in neurons isolated from E16.5 mouse embryonic cortices from WT and SMCX KO mice and harvested after 10 days in vitro culture.
Project description:We conducted ChIP-Seq of H3K4 methylation in neurons isolated from E16.5 mouse embryonic cortices from WT and SMCX KO mice and harvested after 10 days in vitro culture. We sequenced H3K4me1, H3K4me3 ChIP and Input samples from mouse embryonic cortical neurons cultured in vitro for 10 days. Experiments were performed in biological and technical duplicates.
Project description:We conducted RNA-Seq (using Direct Ligation of Adapters to first strand cDNA) in neurons from E16.5 mouse embryonic cortices from WT and SMCX KO mice and harvested after 10 days in vitro culture.
Project description:We conducted RNA-Seq (using Direct Ligation of Adapters to first strand cDNA) in neurons from E16.5 mouse embryonic cortices from WT and SMCX KO mice and harvested after 10 days in vitro culture. We sequenced RNA samples after 10 days in vitro cultures in biological and technical duplicates. 4 RNA samples from WT and SMCX KO neurons. We also sequenced RNA samples from same neurons after stimulation with KCl for 60 mins. So a total of 8 RNA-Seq samples.
Project description:We conducted ChIP-Seq of KDM5c in neurons isolated from E16.5 mouse embryonic cortices from WT and SMCX KO mice and harvested after 10 days in vitro culture.
Project description: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.
Project description: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.
Project description: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.
Project description: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. ChIP-seq for H3K4me3 in wild type and R6/2 cortex and striatum at 8 and 12 weeks.