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Gene expression regulated by let-607 RNAi in C. elegans

ABSTRACT: Gene expression regulated by let-607 RNAi in C. elegans

PROVIDER: PRJNA656126 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12416809_1.fastq.gz	Fastqsanger.gz
	SRR12416809_2.fastq.gz	Fastqsanger.gz
	SRR12416810_1.fastq.gz	Fastqsanger.gz
	SRR12416810_2.fastq.gz	Fastqsanger.gz
	SRR12416811_1.fastq.gz	Fastqsanger.gz

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Gene expression regulated by let-607 RNAi in C. elegans

Project description:Coordinated regulation of stress response pathways is crucial for cellular homeostasis. However, crosstalk between the different stress pathways and the physiological significance of this crosstalk remain poorly understood. In this study, using the model organism C. elegans, we discovered that suppression of the transcription factor LET-607/CREBH, a regulator of cellular defense and proteostatic responses, triggers adaptive induction of DAF-16-dependent stress responses. Suppression of LET-607 improves stress resistance and extends C. elegans lifespan in a DAF-16-dependent manner. We identified the sphingomyelin synthase SMS-5 to be a central mediator in the communication between LET-607 and DAF-16. SMS-5 reduces the contents of unsaturated phosphatidylcholine (PC), which activates DAF-16 through ITR-1-dependent calcium signaling and calcium-sensitive kinase PKC-2. Our data reveal the significance of crosstalk between different stress pathways in animal fitness and identify LET-607/CREBH and specific PC as regulators of DAF-16 and longevity.

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Project description:We resport the changes in gene expression occuring after heat exposure in C. elegans with low s-adenosylmethionine, or RNAi of two H3K4 methyltransferases Using a C. elegans model of low SAM, we previously found that transcriptional responses response to a bacterial pathogen failed and these bacterial-response genes did not show normal H3K4me3 close to the transcriptional start sites, (Ding et al. 2015 Cell Metabolism). We also found the HMT set-16/MLL was required for full induction, whereas set-2/SET1 appeared dispensable (Ding et al. 2015 Cell Metabolism). We hypothesized that animals with low SAM might fail to transcriptionally respond to stress and that the HMTs may also have distinct roles in modulating stress responses. In our present study, we set out to compare induction of transcriptional responses and survival upon stress exposure between C. elegans with reduced SAM (sams-1(RNAi)) and animals with limited H3K4me3 function, set-2/SET1, and set-16/MLL RNAi. Because distinct stresses may rely on different transcriptional activation mechanisms, we also compared whole-genome expression patterns in three stresses: pathogenic bacteria (PA14), xenotoxic (R24) and heat in response to each RNAi.

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