Altered Transcription Factor Binding and Gene Bivalency in Islets of Intrauterine Growth Retarded Rats.

Cells
Yu-Chin LienR A Simmons

Abstract

Intrauterine growth retardation (IUGR), which induces epigenetic modifications and permanent changes in gene expression, has been associated with the development of type 2 diabetes. Using a rat model of IUGR, we performed ChIP-Seq to identify and map genome-wide histone modifications and gene dysregulation in islets from 2- and 10-week rats. IUGR induced significant changes in the enrichment of H3K4me3, H3K27me3, and H3K27Ac marks in both 2-wk and 10-wk islets, which were correlated with expression changes of multiple genes critical for islet function in IUGR islets. ChIP-Seq analysis showed that IUGR-induced histone mark changes were enriched at critical transcription factor binding motifs, such as C/EBPs, Ets1, Bcl6, Thrb, Ebf1, Sox9, and Mitf. These transcription factors were also identified as top upstream regulators in our previously published transcriptome study. In addition, our ChIP-seq data revealed more than 1000 potential bivalent genes as identified by enrichment of both H3K4me3 and H3K27me3. The poised state of many potential bivalent genes was altered by IUGR, particularly Acod1, Fgf21, Serpina11, Cdh16, Lrrc27, and Lrrc66, key islet genes. Collectively, our findings suggest alterations of histone modification in ...Continue Reading

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Datasets Mentioned

BETA
GSE147992

Methods Mentioned

BETA
RNA-Seq
acetylation
Immunoprecipitation
ChIP
PCR
ChIP-Seq
nucleotide exchange

Software Mentioned

Genome
MACS2
QIAGEN
HOMER
Integrative Genomics Viewer ( IGV ) browser
Ingenuity Pathway Analysis ( IPA )
Ingenuity pathway analysis ( IPA
STAR
browser
Trimmomatic

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