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Role of mitochondrial unfolded protein response transcription fatcor ATFS-1 in lifespan of long-lived mitochondrial mutants

ABSTRACT: Role of mitochondrial unfolded protein response transcription fatcor ATFS-1 in lifespan of long-lived mitochondrial mutants

PROVIDER: PRJNA435494 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6761010.fastq.gz	Fastqsanger.gz
	SRR6761020.fastq.gz	Fastqsanger.gz
	SRR6761030.fastq.gz	Fastqsanger.gz
	SRR6761040.fastq.gz	Fastqsanger.gz
	SRR6761011.fastq.gz	Fastqsanger.gz

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Role of mitochondrial unfolded protein response transcription fatcor ATFS-1 in lifespan of long-lived mitochondrial mutants

Project description:In this work, we examined the effect of the transcription factor ATFS-1 in the long lifespan of the nuo-6 mitochondrial mutant. We also examined the effect of the hypoxia transcription factor hif-1. We sequenced both atfs-1 deletion mutants and atfs-1 gain-of-function point mutants in which the mitochondrial localization sequence of ATFS-1 is disrupted. Note that sequencing batch 2 was previously uploaded as part of GSE93724.

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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

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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V-ATPase/TORC1-mediated ATFS-1 translation directs mitochondrial UPR activation in C. elegans

Project description:To adapt mitochondrial function to the ever-changing intra- and extra-cellular environment, multiple mitochondrial stress response (MSR) pathways, including the mitochondrial unfolded protein response (UPRmt), have evolved. However, how the mitochondrial stress signal is sensed and relayed to UPRmt transcription factors, such as ATFS-1 in Caenorhabditis elegans, remains largely unknown. Here, we show that a panel of vacuolar H+-ATPase (v-ATPase) subunits and the target of rapamycin complex 1 (TORC1) activity are essential for the cytosolic relay of mitochondrial stress to ATFS-1, and for the induction of the UPRmt. Mechanistically, mitochondrial stress stimulates v-ATPase/Rheb-dependent TORC1 activation, subsequently promoting ATFS-1 translation. Increased translation of ATFS-1 upon mitochondrial stress furthermore relies on a set of ribosomal components, but is independent of GCN-2/PEK-1 signaling. Finally, the v-ATPase and ribosomal subunits are required for mitochondrial surveillance and mitochondrial stress-induced longevity. These results reveal a v-ATPase-TORC1-ATFS-1 signaling pathway that links mitochondrial stress to the UPRmt through intimate crosstalks between multiple organelles.

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ATFS-1 mediates a protective transcription program during mitochondrial stress

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Investigating impacts of mycothiazole and its synthetic derivative on mitochondrial function and aging in C. elegans

Project description:Small molecule inhibitors of mitochondrial electron transport chain (ETC) hold significant promise in the field of mitochondrial research and aging biology. In this study, we studied two molecules: mycothiazole (MTZ) - isolated from the marine sponge P. mycofijiensis and its semisynthetic acetylated derivative 8-O-acetylmycothiazole (8-OAc) as efficient alternatives for their high efficiency to inhibit ETC complex I function. Similar to rotenone, a widely used complex I inhibitor, these two compounds showed anticancer activity and strikingly demonstrate a lack of toxicity to non-cancer cells, a highly beneficial feature in the development of anti-cancer therapeutics. Furthermore, experiments with these small molecules in vivo utilizing C.elegans demonstrate their additional utilization to aging studies. We observed that both molecules have the ability to induce a mitochondria-specific unfolded protein response (UPRMT) pathway, which extends lifespan of worms when applied in their adult stage. Interestingly, we also found that these two molecules employ different pathways to extend lifespan in worms, where MTZ utilize the transcription factors, ATFS-1 and HSF-1, which are involved in the UPRMT and heat shock response (HSR) pathways, respectively. In opposition,8-OAc only required HSF-1 and not ATFS-1. This observation elucidates an important insight into the functional roles of various protein subunits of ETC complexes and their regulatory mechanisms associated with aging.

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