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ChIP-seq analysis to identify transcriptional targets of BMAL1 mammary epithelial cells in culture, and determine if targets of BMAL1 changed upon lactogen induced differentiation of mammary epithelial cells in culture

ABSTRACT: ChIP-seq analysis was used to identify genes potentially regulated by BMAL1 in undifferentiated (UNDIFF) and lactogen hormone differentiated (DIFF) HC11 cultures. HC11 cells are a normal mouse mammary epithelial cell line. Prior to beginning studies, specificity of the ChIP-grade antibody for the BMAL1 protein was confirmed with immunoprecipitation and western blot analysis. Nanochip analysis of sonicated input DNA indicated that optimal size of sheared fragments was achieved for ChIP-seq analysis. Moreover, ChIP-qPCR analysis of the promoter region of PER1, a transcriptional target of BMAL1:CLOCK, found that 70% of the input DNA sequence was captured by chromatin immunoprecipitation, with the q-PCR product being 9-fold higher in BMAL1-ChIP samples than mock samples (no primary antibody added). Q-PCR analysis of the exon region of MAGEA 1_2, a sperm specific gene that is not a BMAL1:CLOCK target was used as a negative control. There was no difference in amount of MAGEA 1_2 q-PCR between mock-ChIP and BMAL1-ChIP samples, thus further validating the BMAL1-ChIP assay. The eight samples sequenced for these studies consisted of four pairs of input and ChIP samples with two pairs from UNDIFF and two from DIFF HC11 cultures. Mapping rate of reads to the mouse genome across the four paired input-ChIP samples averaged 96%.

ORGANISM(S): Mus musculus

PROVIDER: GSE154937 | GEO | 2021/07/22

REPOSITORIES: GEO

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MYC-associated factor X, MAX, binds BMAL1 targeted genomic regions with high affinity [ChIP-Seq]

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