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Glutathione accelerates the cell cycle and cellular reprogramming in plant regeneration [scRNA-seq]

ABSTRACT: Glutathione accelerates the cell cycle and cellular reprogramming in plant regeneration [scRNA-seq]

PROVIDER: PRJNA1122783 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29364678_1.fastq.gz	Fastqsanger.gz
	SRR29364678_2.fastq.gz	Fastqsanger.gz
	SRR29364679_1.fastq.gz	Fastqsanger.gz
	SRR29364679_2.fastq.gz	Fastqsanger.gz
	SRR29364680_1.fastq.gz	Fastqsanger.gz

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Glutathione accelerates the cell cycle and cellular reprogramming in plant regeneration [bulk RNA-seq]

Project description:Glutathione accelerates the cell cycle and cellular reprogramming in plant regeneration [bulk RNA-seq]

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Glutathione accelerates the cell cycle and cellular reprogramming in plant regeneration [scRNA-seq]

Project description:The plasticity of plant cells underlies their wide capacity to regenerate, with increasing evidence in plants and animals implicating cell cycle dynamics in cellular reprogramming. To investigate the cell cycle during cellular reprogramming, we developed a comprehensive set of cell cycle phase markers in the Arabidopsis root. Using single-cell RNA-seq profiles and live imaging during regeneration, we found that a subset of cells near an ablation injury dramatically increases division rate by truncating G1 phase. Cells in G1 undergo a transient nuclear peak of glutathione (GSH) prior to coordinated entry into S phase followed by rapid divisions and cellular reprogramming. A symplastic block of the ground tissue impairs regeneration, which is rescued by exogenous GSH. We propose a model in which GSH from the outer tissues is released upon injury licensing an exit from G1 near the wound to induce rapid cell division and reprogramming.

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Glutathione accelerates the cell cycle and cellular reprogramming in plant regeneration.

Project description: Not available

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Loss of G9a in myofiber accelerates muscle regeneration

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Loss of G9a in myofiber accelerates muscle regeneration

Project description:Age-related muscle regenerative capacity decline is related to the disruption of the Injured skeletal muscle regenerates through a network orchestrated by multiple muscle-harbored cell types, however, yet the contribution of the interplay between macrophages and myofibers upon injuryto this process is largely unknown. Deletion of G9a in myofiber mitigates muscle aging and accelerates muscle regeneration. Mechanistically, by deleting Osteocrin (musclin-encoding) in myofiber-specific G9a knockout background, we found G9a suppresses myofiber-derived musclin to inhibit myogenesis and macrophage phenotype transition during muscle regeneration.Musclin recombination protein accelerated muscle regeneration. Collectively, we highlight an epigenetic mechanism that links muscle aging to muscle regeneration, G9a serves an epigenetic hallmark of muscle aging and a the crosstalk between myofibers and macrophages , both regulated by G9a, steers a pro-recovery microenvironment after muscle injury, which offers therapeutic potentials for muscle regenerative capacity decline in the aged.

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Mouse sciatic nerve LC-MSMS - Delaying histone deacetylase response to injury accelerates conversion into repair Schwann cells and nerve regeneration

Project description:The peripheral nervous system (PNS) regenerates after injury. However regeneration is often compromised in case of large lesions, the speed of axon reconnection to their target being critical for successful functional recovery. After injury, mature Schwann cells (SCs) convert into repair cells that foster axonal regrowth, and redifferentiate to rebuild myelin. These processes require the regulation of several transcription factors, but the driving mechanisms remain partially understood. Here, we identify an early response to injury controlled by histone deacetylase (HDAC)2, which coordinates the action of other chromatin-remodeling enzymes to induce the upregulation of Oct6, a key transcription factor for Schwann cell development. Inactivating this mechanism using mouse genetics allows earlier conversion into repair cells and leads to faster axonal regrowth, but impairs remyelination. Consistently, short-term HDAC1/2 inhibitor treatment early after lesion accelerates functional recovery and enhances regeneration, thereby identifying a new therapeutic strategy to improve PNS regeneration after lesion.

2018-10-17 | PXD005383 | Pride

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