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

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

PROVIDER: PRJNA1095999 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28549800_1.fastq.gz	Fastqsanger.gz
	SRR28549800_2.fastq.gz	Fastqsanger.gz
	SRR28549801_1.fastq.gz	Fastqsanger.gz
	SRR28549801_2.fastq.gz	Fastqsanger.gz
	SRR28549802_1.fastq.gz	Fastqsanger.gz

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

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