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Mitochondrial respiration maintains autophagy to support stress resistance in quiescent cells

ABSTRACT: Mitochondrial respiration maintains autophagy to support stress resistance in quiescent cells

PROVIDER: PRJNA609070 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11193561_1.fastq.gz	Fastqsanger.gz
	SRR11193561_2.fastq.gz	Fastqsanger.gz
	SRR11193562_1.fastq.gz	Fastqsanger.gz
	SRR11193562_2.fastq.gz	Fastqsanger.gz
	SRR11193563_1.fastq.gz	Fastqsanger.gz

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Mitochondrial respiration maintains autophagy to support stress resistance in quiescent cells

Project description:Mitochondrial oxidative phosphorylation (OXPHOS) generates ATP and is required for pyrimidine nucleotide synthesis during proliferation. In contrast, the role of OXPHOS in post-mitotic cells, beyond its contribution to ATP production, is less understood. Here, we show that in non-proliferating cells, OXPHOS ensures protection against oxidative stress by sustaining autophagy. Autophagy is suppressed and oxidative stress resistance is compromised in OXPHOS-deficient non-proliferating cells in vitro and in TFAM knockout mice in vivo, while attenuation of autophagy in OXPHOS-functional cells phenocopies the effects of OXPHOS deficiency. Mechanistically, the regulation of the autophagy / stress response by OXPHOS does not require changes in gene expression, AMPK/mTOR1/ULK1 signaling or NADH levels. Instead, OXPHOS maintains ROS levels to prevent activation of ATG4, a ROS-activated inhibitor of autophagy. We propose that protection against oxidative stress via the ROS-ATG4 axis is a novel function of mitochondrial respiration in non-proliferating cells that may have consequences for cancer therapy and beyond.

2022-01-07 | GSE146025 | GEO

Mitochondrial respiration is necessary to combat oxidative stress in quiescent cells

Project description:Mitochondrial oxidative phosphorylation (OXPHOS) makes ATP and supports biosynthesis during proliferation, but its role in non-proliferating cells, beyond ATP production, is less understood. Here we show that OXPHOS protects quiescent (but not proliferating) cells from oxidative stress. Using in vivo models of OXPHOS deficiency (whole body and endothelium-specific) we show that OXPHOS mediated resistance to ROS (i) maintains selectivity of ROS-based anticancer therapy by protecting normal tissues during treatment, and in quiescent endothelium (ii) ameliorates systemic LPS-induced inflammation and (iii) attenuates symptoms of the inflammatory bowel disease. ROS-resistance provided by OXPHOS is independent of its role in biosynthesis or NADH recycling. Instead, in quiescent cells OXPHOS constitutively generates low levels of endogenous ROS that support basal autophagic flux and protect from exogenous ROS challenge. Hence, during evolution cells acquired mitochondria to profit from oxidative metabolism, but also built in an OXPHOS-dependent mechanism to guard against the resulting oxidative stress.

2022-10-13 | PXD021376 | Pride

Autophagy maintains intestinal stem cell integrity

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Endothelial ERK1/2 signaling maintains integrity of the quiescent endothelium

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Oncogenic KIT mutations induce STAT3-dependent autophagy to support cell proliferation in acute myeloid leukemia

Project description:Autophagy is associated with both survival and cell death in myeloid malignancies. Therefore, deciphering its role in different genetically defined subtypes of acute myeloid leukemia (AML) is critical. Activating mutations of the KIT receptor tyrosine kinase are frequently detected in core-binding factor AML and are associated with a greater risk of relapse. Herein, we report that basal autophagy was significantly increased by the KITD816V mutation in AML cells and contributed to support their cell proliferation and survival. Invalidation of the key autophagy protein Atg12 strongly reduced tumor burden and improved survival of immunocompromised NSG mice engrafted with KITD816V TF-1 cells. Downstream of KITD816V, STAT3, but not AKT or ERK pathways, was identified as a major regulator of autophagy. Accordingly, STAT3 pharmacological inhibition or downregulation inhibited autophagy and reduced tumor growth both in vitro and in vivo. Taken together, our results support the notion that targeting autophagy or STAT3 opens up an exploratory pathway for finding new therapeutic opportunities for patients with CBF-AML or others malignancies with KITD816V mutations.

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FoxO maintains a genuine quiescent muscle stem-cell state until geriatric age

Project description:FoxO maintains a genuine quiescent muscle stem-cell state until geriatric age

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Autophagy maintains intestinal stem cell integrity

Project description:The intestinal epithelium is continuously renewed by a pool of intestinal stem cells expressing Lgr5. We show that deletion of the key autophagy gene Atg7 affects the survival of Lgr5+ intestinal stem cells. Mechanistically, this involves defective DNA repair, oxidative stress, and altered interactions with the microbiota. This study highlights the importance of autophagy in maintaining the integrity of intestinal stem cells.

2020-05-28 | GSE136952 | GEO

FoxO maintains a genuine quiescent muscle stem-cell state until geriatric age (RNA-seq)

Project description:FoxO maintains a genuine quiescent muscle stem-cell state until geriatric age (RNA-seq)

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