ChIP-seq analysis of KAP1 and H3K9me3 modifications in mouse spleen B cells

ABSTRACT: Chromatin remodeling is fundamental for B cell differentiation. Here, we explored the role in this process of KAP1, the cofactor of KRAB-ZFP transcriptional repressors. B lymphoid-specific Kap1 knockout mice displayed reduced numbers of mature B cells, lower steady-state levels of antibodies and accelerated rates of decay of neutralizing antibodies following viral immunization. Transcriptome analyses of Kap1-deleted B splenocytes revealed an upregulation of PTEN, the enzymatic counter-actor of PIK3 signaling, and of genes encoding DNA damage response factors, cell-cycle regulators and chemokine receptors. ChIP/seq studies established that KAP1 bound at or close to a number of these genes, and controlled chromatin status at their promoters. Genome-wide, KAP1-binding sites avoided active B c

ORGANISM(S): Mus musculus

SUBMITTER: Francesca Santoni de Sio 

PROVIDER: E-GEOD-36850 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress