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Essential Roles of SETD7 as Transcriptional Activator and Co-regulator of H3K36me in Cardiac Lineage Commitment

ABSTRACT: Essential Roles of SETD7 as Transcriptional Activator and Co-regulator of H3K36me in Cardiac Lineage Commitment

PROVIDER: PRJNA421471 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6357560_1.fastq.gz	Fastqsanger.gz
	SRR6357560_2.fastq.gz	Fastqsanger.gz
	SRR6357570.fastq.gz	Fastqsanger.gz
	SRR6357570_1.fastq.gz	Fastqsanger.gz
	SRR6357570_2.fastq.gz	Fastqsanger.gz

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Essential Roles of SETD7 as Transcriptional Activator and Co-regulator of H3K36me in Cardiac Lineage Commitment

Project description:Coordinated epigenome alteration is fundamental for cardiac development. However, the precise mechanisms by which epigenetic modifying enzymes regulate cardiac development are still unclear. Here we identify SET domain containing protein 7 (SETD7) as a key regulator of cardiac differentiation. ChIP-seq reveals that SETD7 has distinct groups of target genes and regulates its stage-specific expression during cardiomyocyte differentiation, which is crucial for lineage commitment. We find SETD7 associates with stage-specific co-factors, such as SWI/SNF chromatin remodeling factors during mesodermal formation and transcription factor NKX2-5 in cardiac progenitor differentiation. Cross-analysis of epigenetic modifications shows that SETD7 recognizes and binds with active histone marker H3K36 methylation on gene-body region of its target genes. We further demonstrate SETD7 is required for functional properties of terminally differentiated cardiomyocytes. Together, our results suggest unidentified roles of SETD7 in cardiac lineage commitment and provide new insights into the crosstalk between epigenetic dynamics and epigenetic modifying enzymes.

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SETD7 functions as a transcription repressor in prostate cancer via methylating FOXA1 [ChIP-seq]

Project description:We recently reported that in prostate cancer LSD1 can demethylate the lysine 270 of FOXA1 to stabilize FOXA1 chromatin binding and thus can enhance the activities of AR and other transcription factors that require FOXA1 as a pioneer factor. However, the methyltransferase that can methylate FOXA1 and negatively regulate the LSD1-FOXA1 oncogenic axis remains unknown. SETD7 is initially identified as a transcriptional activator through methylating histone 3 lysine 4 but can also function as a methyltransferase on other non-histone substrates. However, its function in PCa remains poorly understood. In this study, we found that SETD7 confers tumor suppressor activity in PCa cells and that loss of SETD7 expression is significantly associated with PCa progression and tumor aggressiveness. Mechanistically, we found that SETD7 primarily acts as a transcriptional repressor in CRPC cells by functioning as a methyltransferase of FOXA1-K270 to disrupt FOXA1-mediated transcription. Overall, our study provides novel mechanistic insights into the tumor-suppressive and transcriptional repression activities of SETD7 in mediating PCa progression and therapy resistance.

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Project description:Herein, we demonstrated that the cell lineage commitment is unexpectedly regulated by the novel functions of H2A.X, a histone variant which was only well-known for its role in genome integrity maintenance previously. Surprisingly, only in ESCs but not differentiated cells, H2A.X is specifically targeted to genomic regions encoding early embryonic and extra-embryonic lineage genes to repress their expression. In addition, H2A.X is also enriched at genomic regions sensitive to replication stress and maintains genomic stability thereat. Most interestingly, faithful H2A.X deposition plays critical roles in maintaining both cell lineage commitment and genome integrity in iPSC. In iPSC lines which support the development of "all-iPS" animals, H2A.X deposition faithfully recapitulates the ESC pattern and therefore, the genome stability and cell lineage commitment are maintained. In iPSC lines that fail to support embryonic development, defective H2A.X depositions result in aberrant upregulation of early embryonic and extra-embryonic lineage genes and H2A.X-dependent genome instability. mRNA-Seq of WT ESC and H2A.X KO ESC; and 4N+, 4N- iPSC.

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SETD7 Drives Cardiac Lineage Commitment through Stage-Specific Transcriptional Activation.

Project description:Cardiac development requires coordinated and large-scale rearrangements of the epigenome. The roles and precise mechanisms through which specific epigenetic modifying enzymes control cardiac lineage specification, however, remain unclear. Here we show that the H3K4 methyltransferase SETD7 controls cardiac differentiation by reading H3K36 marks independently of its enzymatic activity. Through chromatin immunoprecipitation sequencing (ChIP-seq), we found that SETD7 targets distinct sets of genes to drive their stage-specific expression during cardiomyocyte differentiation. SETD7 associates with different co-factors at these stages, including SWI/SNF chromatin-remodeling factors during mesodermal formation and the transcription factor NKX2.5 in cardiac progenitors to drive their differentiation. Further analyses revealed that SETD7 binds methylated H3K36 in the bodies of its target genes to facilitate RNA polymerase II (Pol II)-dependent transcription. Moreover, abnormal SETD7 expression impairs functional attributes of terminally differentiated cardiomyocytes. Together, these results reveal how SETD7 acts at sequential steps in cardiac lineage commitment, and they provide insights into crosstalk between dynamic epigenetic marks and chromatin-modifying enzymes.

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