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BMAL1 Modulates Senescence Programming via AP-1.

ABSTRACT: BMAL1 Modulates Senescence Programming via AP-1.

PROVIDER: PRJNA952579 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24085231.fastq.gz	Fastqsanger.gz
	SRR24085231_1.fastq.gz	Fastqsanger.gz
	SRR24085231_2.fastq.gz	Fastqsanger.gz
	SRR24085232.fastq.gz	Fastqsanger.gz
	SRR24085232_1.fastq.gz	Fastqsanger.gz

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BMAL1 Modulates Senescence Programming via AP-1 (BMAL1-ChIP-seq)

Project description:BMAL1 Modulates Senescence Programming via AP-1 (BMAL1-ChIP-seq)

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BMAL1 Modulates Senescence Programming via AP-1 (BMAL1-ChIP-seq)

Project description:Cellular senescence and circadian dysregulation are biological hallmarks of aging. Whether they are interdependent has not been thoroughly studied. We hypothesize that BMAL1, a pioneer transcription factor and master regulator of the molecular circadian clock, plays a role in the senescence program. In this study, we show that BMAL1 in is uniquely localized to genomic motifs associated with AP-1 in senescent cells and contributes to AP-1 transcriptional control of the senescence program.

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BMAL1 Modulates Senescence Programming via AP-1 (WT and Bmal1 KO RNA-seq)

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BMAL1 modulates senescence programming via AP-1.

Project description:Cellular senescence and circadian dysregulation are biological hallmarks of aging. Whether they are coordinately regulated has not been thoroughly studied. We hypothesize that BMAL1, a pioneer transcription factor and master regulator of the molecular circadian clock, plays a role in the senescence program. Here, we demonstrate BMAL1 is significantly upregulated in senescent cells and has altered rhythmicity compared to non-senescent cells. Through BMAL1-ChIP-seq, we show that BMAL1 is uniquely localized to genomic motifs associated with AP-1 in senescent cells. Integration of BMAL1-ChIP-seq data with RNA-seq data revealed that BMAL1 presence at AP-1 motifs is associated with active transcription. Finally, we showed that BMAL1 contributes to AP-1 transcriptional control of key features of the senescence program, including altered regulation of cell survival pathways, and confers resistance to drug-induced apoptosis. Overall, these results highlight a previously unappreciated role of the core circadian clock component BMAL1 on the molecular phenotype of senescent cells.

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BMAL1 Modulates Senescence Programming via AP-1.

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-08-22 | GSE229023 | GEO

Cell State Dependent Effects of Bmal1 on Melanoma Immunity and Tumorigenicity

Project description:The circadian clock regulator Bmal1 modulates tumorigenesis, but its reported effects are often inconsistent. Here, we show that Bmal1 has a context-dependent role in mouse melanoma tumor growth. Loss of Bmal1 in YUMM or B16 melanoma cells eliminated clock function, and diminished hypoxic gene expression signature and tumorigenesis, which could be rescued by ectopic expression of HIF-1a. By contrast, over-expressed wild-type or a dominant negative Bmal1 non-canonically sequestered myosin heavy chain 9 (Myh9) to increase MRTF-SRF activity and AP-1 transcriptional signature, and shift YUMM 2.1 cells from a Sox10high to a Sox9high immune resistant, mesenchymal cell state that is found in human melanomas. Our work uncovers a link between Bmal1, Myh9, mouse melanoma cell plasticity, and tumor immunity. This connection may underlie cancer therapeutic resistance and underpin the link between the circadian clock, MRTF-SRF and the cytoskeleton.

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AP-1 signaling modulates cardiac fibroblast stress responses

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