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Transcriptional repression and enhancer decommissioning silence cell cycle genes in postmitotic tissues: RNA-Seq Timecourse from Developing Drosophila Eye

ABSTRACT: Transcriptional repression and enhancer decommissioning silence cell cycle genes in postmitotic tissues: RNA-Seq Timecourse from Developing Drosophila Eye

PROVIDER: PRJNA1093061 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28491949_1.fastq.gz	Fastqsanger.gz
	SRR28491949_2.fastq.gz	Fastqsanger.gz
	SRR28491950_1.fastq.gz	Fastqsanger.gz
	SRR28491950_2.fastq.gz	Fastqsanger.gz
	SRR28491951_1.fastq.gz	Fastqsanger.gz

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Transcriptional repression and enhancer decommissioning silence cell cycle genes in postmitotic tissues: ATAC-Seq Timecourse from Drosophila Eye and Brain

Project description:Transcriptional repression and enhancer decommissioning silence cell cycle genes in postmitotic tissues: ATAC-Seq Timecourse from Drosophila Eye and Brain

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Transcriptional repression and enhancer decommissioning silence cell cycle genes in postmitotic tissues: RNA-Seq Timecourse from Developing Drosophila Eye

Project description:Previous work in the developing Drosophila wing revealed that cell cycle genes are subject to two types of chromatin regulation. The majority of cell cycle genes exhibit a simple regulatory landscape, with promoters that remain accessible even after cell cycle exit. A few critical, rate-limiting cell cycle genes show a more complex and dynamic landscape, and enhancers near these genes show evidence of decomissioning after cell cycle exit has occurred. Here we address whether the findings made in the wing are applicable to other postmitotic tissues that persist for the lifetime of the animal: the eye and the brain. We find that these tissues show similar chromatin accessibility profiles at cell cycle genes, suggesting that these modes of regulation are shared across tissues and that multiple strategies support cell cycle gene repression in the postmitotic state. These include stable repression at the promoters of most cell cycle genes, combined with enhancer decommissioning at a few select, rate-limiting genes.

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Transcriptional repression and enhancer decommissioning silence cell cycle genes in postmitotic tissues: ATAC-Seq Timecourse from Drosophila Eye and Brain

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Transcriptional repression and enhancer decommissioning silence cell cycle genes in postmitotic tissues

Project description:Transcriptional repression and enhancer decommissioning silence cell cycle genes in postmitotic tissues

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Transcriptional repression and enhancer decommissioning silence cell cycle genes in postmitotic tissues.

Project description:The mechanisms that maintain a non-cycling status in postmitotic tissues are not well understood. Many cell cycle genes have promoters and enhancers that remain accessible even when cells are terminally differentiated and in a non-cycling state, suggesting their repression must be maintained long term. In contrast, enhancer decommissioning has been observed for rate-limiting cell cycle genes in the Drosophila wing, a tissue where the cells die soon after eclosion, but it has been unclear if this also occurs in other contexts of terminal differentiation. In this study, we show that enhancer decommissioning also occurs at specific, rate-limiting cell cycle genes in the long-lived tissues of the Drosophila eye and brain, and we propose this loss of chromatin accessibility may help maintain a robust postmitotic state. We examined the decommissioned enhancers at specific rate-limiting cell cycle genes and showed that they encode for dynamic temporal and spatial expression patterns that include shared, as well as tissue-specific elements, resulting in broad gene expression with developmentally controlled temporal regulation. We extend our analysis to cell cycle gene expression and chromatin accessibility in the mammalian retina using a published dataset and find that the principles of cell cycle gene regulation identified in terminally differentiating Drosophila tissues are conserved in the differentiating mammalian retina. We propose a robust, non-cycling status is maintained in long-lived postmitotic tissues through a combination of stable repression at most cell cycle genes, alongside enhancer decommissioning at specific rate-limiting cell cycle genes.

| S-EPMC11457063 | biostudies-literature

Transcriptional repression and enhancer decommissioning silence cell cycle genes in postmitotic tissues

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

2024-04-26 | GSE263160 | GEO

Mi-2 and E93 coordinate robust cell cycle exit with terminal differentiation through enhancer decommissioning [RNA-seq]

Project description:Many postmitotic tissues coordinate robust cell cycle exit with the progression of terminal differentiation. While the signals involved in initiating cell cycle exit during terminal differentiation for some tissues have been described, less is known about the mechanisms that maintain a stable, non-cycling state. We previously found that chromatin accessibility changes at a subset of rate-limiting cell cycle genes occurs during maintenance of cell cycle exit, suggesting chromatin remodelers may play a key role in maintaining a robust postmitotic state during terminal differentiation. Here we show that the chromatin remodeler Mi-2 is required to ensure a stable, postmitotic state in Drosophila eyes and wings. Mi-2 alters chromatin accessibility and gene expression during cell cycle exit and terminal differentiation. Mi-2 and a transcription factor involved in tissue maturation, E93, close chromatin accessibility at an overlapping subset of potential enhancers that include the rate-limiting mitotic regulator string (cdc25c) and genes involved in the progression of terminal differentiation. E93 is also required for a stable, postmitotic state and we verified in vivo that Mi-2 and E93 cooperate to decommission an enhancer for the essential mitotic regulator string, to coordinate the transition to a postmitotic state with terminal differentiation. Enhancer decommissioning at the string locus provides a molecular explanation for the long-term, nearly irreversible postmitotic state observed in many tissues as terminal differentiation progresses.

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