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FNDC-1-Mediated Mitophagy and ATFS-1 Coordinate to Protect Against Hypoxia-Reoxygenation

ABSTRACT: FNDC-1-Mediated Mitophagy and ATFS-1 Coordinate to Protect Against Hypoxia-Reoxygenation

PROVIDER: PRJNA666012 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12721322.fastq.gz	Fastqsanger.gz
	SRR12721323.fastq.gz	Fastqsanger.gz
	SRR12721324.fastq.gz	Fastqsanger.gz
	SRR12721325.fastq.gz	Fastqsanger.gz
	SRR12721326.fastq.gz	Fastqsanger.gz

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FNDC-1-Mediated Mitophagy and ATFS-1 Coordinate to Protect Against Hypoxia-Reoxygenation

Project description:Mitochondrial Quality Control (MQC) balances organelle adaptation and elimination, and mechanistic crosstalk between the underlying molecular processes impacts subsequent stress outcomes. FUN14 Domain Containing 1 (FUNDC1) is a mammalian mitophagy receptor that responds to hypoxia-reoxygenation (HR) stress. Here, we provide evidence that FNDC-1 is the C. elegans ortholog of FUNDC1, and that its loss protects against injury in a worm model of HR. This protection depends upon ATFS-1, a transcription factor that is central to the mitochondrial unfolded protein response (UPRmt). Global mRNA and metabolite profiling suggest that atfs-1 dependent stress responses and metabolic remodeling occur in response to the loss of fndc-1. These data support a role for FNDC-1 in non-hypoxic MQC, and further suggest that these changes are prophylactic in relation to subsequent HR. Our results highlight functional coordination between mitochondrial adaptation and elimination that organizes stress responses and metabolic rewiring to protect against HR injury.

2021-09-01 | GSE158628 | GEO

FNDC-1-mediated mitophagy and ATFS-1 coordinate to protect against hypoxia-reoxygenation.

Project description:Mitochondrial quality control (MQC) balances organelle adaptation and elimination, and mechanistic crosstalk between the underlying molecular processes affects subsequent stress outcomes. FUNDC1 (FUN14 domain containing 1) is a mammalian mitophagy receptor that responds to hypoxia-reoxygenation (HR) stress. Here, we provide evidence that FNDC-1 is the C. elegans ortholog of FUNDC1, and that its loss protects against injury in a worm model of HR. This protection depends upon ATFS-1, a transcription factor that is central to the mitochondrial unfolded protein response (UPRmt). Global mRNA and metabolite profiling suggest that atfs-1-dependent stress responses and metabolic remodeling occur in response to the loss of fndc-1. These data support a role for FNDC-1 in non-hypoxic MQC, and further suggest that these changes are prophylactic in relation to subsequent HR. Our results highlight functional coordination between mitochondrial adaptation and elimination that organizes stress responses and metabolic rewiring to protect against HR injury.Abbreviations: AL: autolysosome; AP: autophagosome; FUNDC1: FUN14 domain containing 1; HR: hypoxia-reperfusion; IR: ischemia-reperfusion; lof: loss of function; MQC: mitochondrial quality control; PCA: principle component analysis; PPP: pentonse phosphate pathway; proK (proteinase K);UPRmt: mitochondrial unfolded protein response; RNAi: RNA interference.

| S-EPMC8632273 | biostudies-literature

ATFS-1 regulates a broad protective transcriptional program

Project description:We previously identified a number of genes which were differentially expressed during mitochondrial stress in an ATFS-1-dependent manner using an atfs-1 loss-of-function mutant allele . To complement the findings from our previous microarray, we compared the transcript profiles from wild-type and atfs-1(et18) gain-of-function worms (which have constitutively active ATFS-1) in the absence of mitochondrial stress. We used microarrays to identify genes regulated by ATFS-1 using a gain-of-function allele of atfs-1.

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DEK deficiency suppresses mitophagy to protect against house dust mite-induced asthma

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ATFS-1 mediates a protective transcription program during mitochondrial stress

Project description:ATFS-1 has been shown to regulate transcription of mitochondrial chaperone genes such as mtHsp70/hsp-6 and hsp-60 in response to mitocondrial stress. To identify the entire ATFS-1-mediated response, we compared the transcript profiles from wild-type and atfs-1(tm4525) worms raised in the absence and presence of mitochondrial stress. We used microarrays to identify genes regulated by ATFS-1 during mitochondrial stress RNA samples were prepared from wild-type(wt) and atfs-1(tm4525)(mutant) worms fed either control(RNAi) or spg-7(RNAi). Worms were synchronized by bleaching, raised in liquid culture and harvested at the L4 stage. Control is denoted as C and spg-7 treatment is denoted T. Each experiment was performed in triplicate indicated as 1,2 and 3.

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To identify ATFS-1 target genes during mitochondrial stress

Project description:To better understand genome coordination and OXPHOS recovery during mitochondrial dysfunction, we examined ATFS-1, a transcription factor that regulates mitochondria-to nuclear communication during the mitochondrial UPR, via ChIP-sequencing. Wildtype worms treated spg-7(RNAi) are analyzed in the presence and absence of ATFS-1 antibody to identify ATFS-1 targets. Individual samples were analyzed. Wildtype worms treated spg-7(RNAi) in the absence of antibody is used as a control.

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ATFS-1 mediates a protective transcription program during mitochondrial stress

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Project description:Ischemia lead to neuronal injury. Dexmedetomidine and astrocytes are likely to protect neuronal cells against ischemia-induced injury. We used microarrays to examine the gene expression variation in astrocytes activated by oxygen-glucose deprivation and reoxygenation stress and identified distinct classes of genes up- and down-regulated by dexmedetomidine pretreatment.

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CLUH-dependent RNA granules coordinate mitochondrial catabolic pathways with mTORC1 signaling and mitophagy

Project description:Mitochondria house anabolic and catabolic processes that must be balanced and rapidly adjusted to meet the cellular demands. CLUH binds mRNAs of nuclear encoded mitochondrial proteins and is highly expressed in the liver, where it regulates metabolic plasticity by an ill-defined mechanism. Here, we show that CLUH-dependent regulation of mitochondrial function is spatially organized through the coalescence of CLUH and its target mRNAs in specific G3BP1-positive granules. These CLUH-dependent granules protect mRNAs involved in mitochondrial energy-converting pathways from decay and define their translational fate to match nutrient availability. CLUH granules suppress premature mTORC1 activation during nutrient deprivation, inhibiting mitochondrial anabolic pathways. Lack of spatial CLUH regulation causes mTORC1 hyperactivation, which impairs mitophagy and triggers cell death. Our data demonstrate that the temporal catabolic adaptation of mitochondria depends on a compartmentalized CLUH-dependent post-transcriptional mechanism that controls mTORC1 signaling and mitochondrial turnover, thus ensuring survival.

2020-03-19 | PXD014098 | Pride

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