C. elegans stress-induced gene expression in low SAM or after histone-methytransferase RNAi
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA497517 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10340338.fastq.gz | Fastqsanger.gz | |||
| SRR10340339.fastq.gz | Fastqsanger.gz | |||
| SRR8079470.fastq.gz | Fastqsanger.gz | |||
| SRR8079480.fastq.gz | Fastqsanger.gz | |||
| SRR8079490.fastq.gz | Fastqsanger.gz |
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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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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.
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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:S-adenosylmethionine (SAM), produced by SAM synthases, is critical for various cellular regulatory pathways and the synthesis of diverse metabolites. Studies have often equated the effects of knocking down one synthase with broader SAM-dependent outcomes such as histone methylation or phosphatidylcholine (PC) production. However, many organisms express multiple synthase genes including humans and Caenorhabditis elegans. Evidence in C. elegans, which possesses an expanded family of SAM synthases, suggest that the enzymatic source of SAM impacts its function. For instance, loss of sams-1 leads to enhanced heat shock survival and increased lifespan, whereas reducing sams-4 adversely affects heat stress survival. Here, we reveal that loss of sams-1 exerts age-dependent effects on nuclear-encoded mitochondrial gene expression, mitochondrial metabolites, and mitophagy. Notably, we find that that SAMS-1 exerts synthase-specific effects on PC production. We propose a mechanistic framework wherein the reduced SAM from SAMS-1 acts through PC to impact mitochondrial fission and mitophagy, thereby enhancing survival during heat stress. This study highlights multifaceted roles of SAM across metabolic pathways and synthase-specific SAM functions.
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Project description:S-adenosylmethionine (SAM), produced by SAM synthases, is critical for various cellular regulatory pathways and the synthesis of diverse metabolites. Studies have often equated the effects of knocking down one synthase with broader SAM-dependent outcomes such as histone methylation or phosphatidylcholine (PC) production. However, many organisms express multiple synthase genes including humans and Caenorhabditis elegans. Evidence in C. elegans, which possesses an expanded family of SAM synthases, suggest that the enzymatic source of SAM impacts its function. For instance, loss of sams-1 leads to enhanced heat shock survival and increased lifespan, whereas reducing sams-4 adversely affects heat stress survival. Here, we reveal that loss of sams-1 exerts age-dependent effects on nuclear-encoded mitochondrial gene expression, mitochondrial metabolites, and mitophagy. Notably, we find that that SAMS-1 exerts synthase-specific effects on PC production. We propose a mechanistic framework wherein the reduced SAM from SAMS-1 acts through PC to impact mitochondrial fission and mitophagy, thereby enhancing survival during heat stress. This study highlights multifaceted roles of SAM across metabolic pathways and synthase-specific SAM functions.
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Project description:A SWATH-based worflow has been developed for C. elegans proteome profiling, including sample preparation, SWATH spectral library generation and downstream data treatment. The influence of mrps-5 RNAi treatment on C. elegans total proteome were studied.
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Project description:Little is known about transcriptional control of neurite branching or presynaptic differentiation, events that occur relatively late in neuronal development. Using the C. elegans mechanosensory circuit as an in vivo model, we show that SAM-10, an ortholog of mammalian Single-Stranded DNA binding Protein (SSDP), functions cell-autonomously in the nucleus to regulate synaptic differentiation as well as positioning of a single neurite branch. PLM mechanosensory neurons in sam-10 mutants exhibit abnormal placement of the neurite branch point, and defective synaptogenesis, characterized by an overextended synaptic varicosity, underdeveloped synaptic morphology and disrupted co-localization of active zone and synaptic vesicles. SAM-10 functions coordinately with LDB-1 (Lim Domain Binding protein-1), demonstrated by our observations that 1) mutations in either gene show similar defects in PLM neurons; and 2) LDB-1 is required for SAM-10 nuclear localization. SAM-10 regulates PLM synaptic differentiation by suppressing transcription of prk-2, which encodes an ortholog of the mammalian Pim kinase family. PRK-2-mediated activities of SAM-10 are specifically involved in PLM synaptic differentiation, but not other sam-10 phenotypes such as neurite branching. Thus, these data reveal a novel transcriptional signaling pathway that regulates neuronal specification of neurite branching and presynaptic differentiation.
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