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Hsf3 governs intramitochondrial ROS homeostasis via regulating respiratory process [ChIP-Seq]

ABSTRACT: Hsf3 governs intramitochondrial ROS homeostasis via regulating respiratory process [ChIP-Seq]

PROVIDER: PRJNA759577 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15687212_1.fastq.gz	Fastqsanger.gz
	SRR15687212_2.fastq.gz	Fastqsanger.gz
	SRR15687213_1.fastq.gz	Fastqsanger.gz
	SRR15687213_2.fastq.gz	Fastqsanger.gz
	SRR15687214_1.fastq.gz	Fastqsanger.gz

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Hsf3 governs intramitochondrial ROS homeostasis via regulating respiratory process

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Hsf3 governs intramitochondrial ROS homeostasis via regulating respiratory process [ChIP-Seq]

Project description:Mitochondrial quality control is essential in modulating intramitochondrial ROS (mtROS) homeostasis that is a critical determinant for many human disorders. Here we identified an atypical function of a heat shock factor, Hsf3, as an important mtROS regulator. Despite HSFs are nuclear proteins and master regulators of protein unfolded response (UPR) across taxa, we demonstrate that Hsf3 is a both nuclei and mitochondria targeting transcription factor that plays an irrelevant function in controlling UPR process. Instead, Hsf3 represses TCA cycle genes and simultaneously regulates electron transfer chain genes encoded from both nuclei and mitochondria. Moreover, both nuclear and mitochondrial targeting signal are required for promising Hsf3 function. Hsf3 regulation responds to multiple intramitochondrial stresses, which activates and ameliorates Hsf3 DNA binding via oxidation of the cysteine residue on DNA binding domain of Hsf3. Collectively, our findings reveal a previously unknown role of HSF family in modulation of mitochondrial function and damage.

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Hsf3 governs intramitochondrial ROS homeostasis via regulating respiratory process [RNA-Seq]

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Project description:Mitochondrial quality control prevents accumulation of intramitochondrial-derived reactive oxygen species (mtROS), thereby protecting cells against DNA damage, genome instability, and programmed cell death. However, underlying mechanisms are incompletely understood, particularly in fungal species. Here, we show that Cryptococcus neoformans heat shock factor 3 (CnHsf3) exhibits an atypical function in regulating mtROS independent of the unfolded protein response. CnHsf3 acts in nuclei and mitochondria, and nuclear- and mitochondrial-targeting signals are required for its organelle-specific functions. It represses the expression of genes involved in the tricarboxylic acid cycle while promoting expression of genes involved in electron transfer chain. In addition, CnHsf3 responds to multiple intramitochondrial stresses; this response is mediated by oxidation of the cysteine residue on its DNA binding domain, which enhances DNA binding. Our results reveal a function of HSF proteins in regulating mtROS homeostasis that is independent of the unfolded protein response.

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