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Comparison of R24 responsive gene expression after histone methyltransferase RNAi in C. elegans

ABSTRACT: Comparison of R24 responsive gene expression after histone methyltransferase RNAi in C. elegans

PROVIDER: PRJNA497521 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8079490.fastq.gz	Fastqsanger.gz
	SRR8079500.fastq.gz	Fastqsanger.gz
	SRR8079491.fastq.gz	Fastqsanger.gz
	SRR8079501.fastq.gz	Fastqsanger.gz
	SRR8079492.fastq.gz	Fastqsanger.gz

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Comparison of heat responsive gene expression after histone methyltransferase RNAi in C. elegans

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Comparison of heat responsive gene expression after histone methyltransferase RNAi in C. elegans

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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Comparison of R24 responsive gene expression after histone methyltransferase RNAi in C. elegans

Project description:We resport the changes in gene expression occuring after R24 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.

2018-10-20 | GSE121509 | GEO

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Project description:We resport the changes in gene expression occuring after Pseudomonas 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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Project description:Gene expression was compared from adult C. elegans after RNAi

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Project description:Hsp90 RNAi in C. elegans

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Total Proteome Analysis in RNAi treated C. elegans (mrps5, fzo1, drp1, eat3)

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