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Chromatin protein profiling during the mammalian cell cycle reveals the extent of mitotic preservation of the regulatory landscape

ABSTRACT: Chromatin protein profiling during the mammalian cell cycle reveals the extent of mitotic preservation of the regulatory landscape

PROVIDER: PRJNA417010 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6251840.fastq.gz	Fastqsanger.gz
	SRR6251841_1.fastq.gz	Fastqsanger.gz
	SRR6251841_2.fastq.gz	Fastqsanger.gz
	SRR6251842_1.fastq.gz	Fastqsanger.gz
	SRR6251842_2.fastq.gz	Fastqsanger.gz

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Chromatin protein profiling during the mammalian cell cycle reveals the extent of mitotic preservation of the regulatory landscape

Project description:We report a novel method to quantify bulk changes of chromatin associated proteins in different cellular states and apply it to the mammalian cell cycle

2018-09-05 | GSE106482 | GEO

Chromatin protein profiling during the mammalian cell cycle reveals the extent of mitotic preservation of the regulatory landscape

Project description:While regulation of transcription, replication and cell division relies on dynamic protein binding to DNA and chromatin, it is unclear which regulatory components remain bound to compacted mitotic chromosomes. To comprehensively quantify the chromatin-associated proteome in different phases of the cell cycle, we utilized the buoyant density of DNA-protein complexes after crosslinking. This revealed variable associations for thousands of proteins to DNA including their frequent and variable phosphorylation. While epigenetic modifiers that promote transcription are lost from mitotic chromatin, repressive modifiers generally remain associated. Interestingly, while proteins involved in transcriptional elongation are evicted, most identified transcription factors are retained on mitotic chromatin to varying degrees, including core promoter binding proteins. This predicts conservation of the regulatory landscape on mitotic chromosomes, which genome-wide measurements of chromatin accessibility confirm. This work establishes a novel approach to study chromatin, provides a comprehensive catalogue of chromatin changes during the cell cycle, and reveals the degree with which the genomic regulatory landscape is maintained through mitosis.

2018-09-06 | PXD008033 | Pride

Cell cycle-resolved chromatin proteomics reveals the extent of mitotic preservation of the genomic regulatory landscape.

Project description:Regulation of transcription, replication, and cell division relies on differential protein binding to DNA and chromatin, yet it is unclear which regulatory components remain bound to compacted mitotic chromosomes. By utilizing the buoyant density of DNA-protein complexes after cross-linking, we here develop a mass spectrometry-based approach to quantify the chromatin-associated proteome at separate stages of the cell cycle. While epigenetic modifiers that promote transcription are lost from mitotic chromatin, repressive modifiers generally remain associated. Furthermore, while proteins involved in transcriptional elongation are evicted, most identified transcription factors are retained on mitotic chromatin to varying degrees, including core promoter binding proteins. This predicts conservation of the regulatory landscape on mitotic chromosomes, which we confirm by genome-wide measurements of chromatin accessibility. In summary, this work establishes an approach to study chromatin, provides a comprehensive catalog of chromatin changes during the cell cycle, and reveals the degree to which the genomic regulatory landscape is maintained through mitosis.

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Cell cycle-dependent YTHDF2 promotes mitotic entry by repressing WEE1

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Cell cycle-dependent YTHDF2 promotes mitotic entry by repressing WEE1

Project description:The m6A modification regulates mRNA stability and translation. Here we show that transcriptomic m6A modification is dynamic and the m6A reader protein YTHDF2 promotes mRNA decay during the cell cycle. Depletion of YTHDF2 leads to the delay of mitotic entry due to overaccumulation of WEE1, a negative regulator of CDK1. We demonstrate that WEE1 transcripts contain m6A modification, which promotes their decay through the m6A reader YTHDF2. Moreover, we found that YTHDF2 protein stability is dependent on CDK1 activity. Thus, CDK1, YTHDF2, and WEE1 form a feedforward regulatory loop to promote mitotic entry. We further identified CUL1, CUL4A, DDB1, and SKP2 as components of E3 ubiquitin ligase complexes that mediate YTHDF2 proteolysis. Our study provides insights into how cell cycle mediators modulate transcriptomic m6A modification, which in turn regulates the cell cycle.

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