Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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ChIP-Seq of Dazl in mouse embryonic stem cells

ABSTRACT: We developed a method to identify chromatin-associated proteins by mass spectrometry. In addition to many known DNA and chromatin-binders, we identified several RNA-binding proteins in the chromatin composition of mouse embryonic stem cells (mESC). Interestingly, we found Dazl as a RBP that specifically binds to chromatin in mESC grown in 2iL condition. So far, Dazl was reported as a RBP that regulates the stability of transcripts in cytoplasm. To identify the binding sites of Dazl on the genome, we carried out a ChIP-seq experiment. As a result, we detected about 1300 reproducible Dazl ChIP-seq peaks. Interestingly, most of the peaks are located close to the transcription start sites of developmental and pluripotency-related genes.

INSTRUMENT(S): Illumina HiSeq 4000

ORGANISM(S): Mus musculus

SUBMITTER: Mahmoud-reza Rafiee

PROVIDER: E-MTAB-9302 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Interaction of the Kaposi’s sarcoma-associated herpesvirus (KSHV) Rta protein with the cellular Notch signaling effector, Recombination Signaling Protein (RBP)-Jk (aka CSL and CBF-1), is essential for viral reactivation from latency. We previously showed that Rta binds to a DNA motif repeated in the viral Mta promoter (called “CANT” or Rta-c) to stimulate RBP-Jk DNA binding, and distinguished Rta from the activated Notch-1 protein. To determine whether Rta’s mechanism would apply generally to other viral promoters, we employed chromatin immunoprecipitation/deep sequencing (ChIP/Seq) to identify Rta and RBP-Jk binding sites across the KSHV genome. We show that RBP-Jk binds nearly exclusively to unique genome sites during latency and reactivation. Many, but not all, reactivation-specific RBP-Jk peaks were associated with Rta bound to single Rta-c motifs. Other motifs that were over-represented with stimulated RBP-Jk DNA binding including those for the cellular DNA binding proteins BCL11A, MNT, MAF B, and TCF12. Four of the top seven motifs that were most over-represented with inhibition of RBP-Jk DNA binding were putative binding sites for the Pit/Oct/Unc (POU) family of proteins, including POU3F3 (Oct-8) and POU5F1 (Oct-4). Interestingly, two other POU motifs, including one for the POU2F1 (Oct-1) protein, are associated with inhibition of RBP-Jk DNA binding unless Rta bound to a nearby Rta-c motif. The relative distances between the Rta-c, POU, and RBP-Jk motifs were conserved at reactivation-specific RBP-Jk peaks in three promoters that Rta transactivated, and the Rta-c and Oct-1 motifs overlapped in two of those. The proximity of the Rta-c/Oct-1 motif to an RBP-Jk motif is critical for Rta transactivation of the ORF50AS/KbZIP promoter, and knockdown of Oct-1 protein debilitated reactivation and production of infectious virus. Our data suggest a broad role for POU proteins in regulating DNA binding of RBP-Jk and its associated transactivators.

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ChIP-Seq of Dazl in mouse embryonic stem cells

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