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C. elegans: wildtype vs nhr-49-/-; wildtype vs nhr-66-/-; wildtype vs nhr-80-/-

ABSTRACT: Transcriptional profiling of C. elegans NHR-49, NHR-66 and NHR-80

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE34856 | GEO | 2012/03/15

SECONDARY ACCESSION(S): PRJNA150119

REPOSITORIES: GEO

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C. elegans: wildtype vs nhr-49-/-; wildtype vs nhr-66-/-; wildtype vs nhr-80-/-

Project description:Transcriptional profiling of C. elegans NHR-49, NHR-66 and NHR-80 Independent data sets were generated for each mutant vs wildtpe comparison: NHR-49 (N=2), NHR-66 (N=3), NHR-80 (N=4)

2012-03-15 | E-GEOD-34856 | biostudies-arrayexpress

NHR-49 controls a HIF-1 independent hypoxia adaptation pathway in Caenorhabditis elegans

Project description:The response to insufficient oxygen, termed hypoxia, is orchestrated by the conserved master regulator Hypoxia-Inducible Factor-1 (HIF-1), which is hyperactive in many cancers. Here, we describe a HIF-1 independent hypoxia response pathway controlled by Caenorhabditis elegans Nuclear Hormone Receptor NHR-49, an orthologue of mammalian lipid metabolism regulator Peroxisome Proliferator-Activated Receptor alpha (PPARα). nhr-49 is required for worm survival in hypoxia and is synthetically lethal with hif-1 in this context, demonstrating independent activity. RNA-seq data show that nhr-49 regulates a set of hif-1 independent hypoxia responsive genes, including autophagy genes that promote hypoxia survival. We further identified the Nuclear Hormone Receptor nhr-67 as a negative regulator and the Homeodomain-interacting Protein Kinase hpk-1 as a positive regulator in the NHR-49 pathway. Together, our experiments describe an essential hypoxia response pathway controlled by nhr-49 that includes new upstream and downstream components and is as important as hif-1 dependent hypoxia adaptation.

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Caenorhabditis elegans

Project description:C. elegans: wildtype vs nhr-49-/- wildtype vs nhr-66-/- wildtype vs nhr-80-/-

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Nuclear receptor NHR-49 promotes peroxisome proliferation to compensate for aldehyde dehydrogenase deficiency in C. elegans

Project description:The intracellular level of fatty aldehydes is tightly regulated to minimize the formation of toxic aldehyde adducts of cellular components. Accordingly, deficiency of a fatty aldehyde dehydrogenase FALDH causes the neurologic disorder Sjögren-Larsson syndrome (SLS) in humans. However, cellular responses to unresolved, elevated fatty aldehyde levels are poorly understood. Based on lipidomic and imaging analysis, we report that the loss of endoplasmic reticulum-, mitochondria- and peroxisomes-associated ALH-4, the C. elegans FALDH ortholog, increases fatty aldehyde levels and reduces fat storage. ALH-4 deficiency in the intestine, cell-nonautonomously induces NHR-49/NHR-79-dependent hypodermal peroxisome proliferation. This is accompanied by the upregulation of catalases and fatty acid catabolic enzymes, as indicated by RNA sequencing. Such a response is required to counteract ALH-4 deficiency since alh-4; nhr-49 double mutant animals are not viable. Our work reveals unexpected inter-tissue communication of fatty aldehyde levels, and suggests pharmacological modulation of peroxisome proliferation as a therapeutic strategy for SLS.

2021-06-07 | GSE162792 | GEO

NHR-49/HNF4 integrates regulation of fatty acid metabolism with a protective transcriptional response to oxidative stress and fasting

Project description:Endogenous and exogenous stresses elicit transcriptional responses that limit damage and promote cell/organismal survival. Like its mammalian counterparts, Hepatocyte Nuclear Factor 4 (HNF4) and peroxisome proliferator-activated receptor a (PPARa), Caenorhabditis elegans NHR-49 is a well-established regulator of lipid metabolism. Here, we reveal that NHR-49 is essential to activate a transcriptional response common to organic peroxide and fasting, which includes the pro-longevity gene fmo-2/flavin-containing monoxygenase. These NHR-49-dependent, stress-responsive genes are also upregulated in long-lived glp-1/notch receptor mutants, and two of them contribute to increased oxidative stress resistance in wild-type worms and long-lived glp-1 mutants. Similar to its role in lipid metabolism, NHR-49 requires the Mediator subunit mdt-15 to promote stress-induced gene expression. However, NHR-49 acts independently from the transcription factor hlh-30/TFEB that also promotes fmo-2 expression. Similarly, activation of the p38 MAPK, PMK-1, which is important for adaptation to a variety of stresses, is only important for peroxide-induced expression of a subset of NHR-49-dependent genes, including fmo-2. Notably, we find that organic peroxide increases NHR-49 protein levels, apparently by a post-transcriptional mechanism that does not require PMK-1 activation. Together these findings establish a new role for the HNF4/PPARa-related NHR-49 as a stress-activated regulator of cytoprotective gene expression.

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RNA-Sequencing used to identify the targets of NHR-49, a transcription factor that acts in distinct tissues to promote longevity versus immunity

Project description:Previously, we identified NHR-49, functional homolog of the key vertebrate lipid metabolism regulator HNF4/PPARa, as essential for the longevity of Germiline Strem Cell (GSC)-less animals. Since longevity and stress resistance have been reported to be strongly linked, we examined the role of NHR-49 in resistance against the human opportunistic pathogen Pseudomonas aeruginosa, strain PA14. As a part of this effort we employed RNA-Sequencing to determine the downstream targets of NHR-49 in GSC-less animals.

2020-09-30 | GSE158729 | GEO

NHR-49 controls a HIF-1 independent hypoxia adaptation pathway in Caenorhabditis elegans

Project description:NHR-49 controls a HIF-1 independent hypoxia adaptation pathway in Caenorhabditis elegans

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RNA-seq analysis of NHR-23-depleted, SPE-44-depleted, and NHR-23+SPE-44-depleted C. elegans

Project description:We performed RNA-seq analysis of control, NHR-23-depleted, SPE-44-depleted and NHR-23+SPE-44 depleted adult male animals, to identify genes regulated by NHR-23 and SPE-44.

2022-06-22 | GSE206676 | GEO

Nuclear receptor NHR-49 promotes peroxisome proliferation to compensate for aldehyde dehydrogenase deficiency in C. elegans

Project description:Nuclear receptor NHR-49 promotes peroxisome proliferation to compensate for aldehyde dehydrogenase deficiency in C. elegans

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Nuclear receptors NHR-49 and NHR-79 promote peroxisome proliferation to compensate for aldehyde dehydrogenase deficiency in C. elegans.

Project description:The intracellular level of fatty aldehydes is tightly regulated by aldehyde dehydrogenases to minimize the formation of toxic lipid and protein adducts. Importantly, the dysregulation of aldehyde dehydrogenases has been implicated in neurologic disorder and cancer in humans. However, cellular responses to unresolved, elevated fatty aldehyde levels are poorly understood. Here, we report that ALH-4 is a C. elegans aldehyde dehydrogenase that specifically associates with the endoplasmic reticulum, mitochondria and peroxisomes. Based on lipidomic and imaging analysis, we show that the loss of ALH-4 increases fatty aldehyde levels and reduces fat storage. ALH-4 deficiency in the intestine, cell-nonautonomously induces NHR-49/NHR-79-dependent hypodermal peroxisome proliferation. This is accompanied by the upregulation of catalases and fatty acid catabolic enzymes, as indicated by RNA sequencing. Such a response is required to counteract ALH-4 deficiency since alh-4; nhr-49 double mutant animals are sterile. Our work reveals unexpected inter-tissue communication of fatty aldehyde levels and suggests pharmacological modulation of peroxisome proliferation as a therapeutic strategy to tackle pathology related to excess fatty aldehydes.

| S-EPMC8291716 | biostudies-literature

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