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Species » C. elegans(Genome assembly: WBcel235)

Expression cluster » WBPaper00062305:P.brevicompactum_upregulated

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  • Overview

    WBPaper00062305:P.brevicompactum_upregulated

    Species:
    Caenorhabditis elegans
    WormBase ID:
    WBPaper00062305:P.brevicompactum_upregulated
    Transcripts that showed significantly increased expression after L1 stage N2 animals were grown on plates covered by mold Penicillium brevicompacum with E. coli OP50 for 48 hours at 20 centigrade.

    Algorithm:

    voom from limma v 3.42.2 was applied to estimate fold changes and BH-adjusted p-values.

    Remarks:

    Type: Fungi Infection

  • Regulation

    Regulated by Gene:
    Regulated by Treatment:
    Fungi infection: Penicillium brevicompacum
    Regulated by Molecule:

  • Associations

    Anatomy Terms:
    Life Stages:
    Life Stages Definition
    1-day post-L4 adult hermaphrodite CeAt 20 Centigrade: 24-48 hours after L4-adult molt. 4-5 days after first cleavage.
    GO terms:
    Processes:

  • References

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      • Journal article

      1

    1 reference found
    Nuclear hormone receptors promote gut and glia detoxifying enzyme induction and protect C.elegans from the mold P.brevicompactum.
    Journal article
    Cell Rep
    2021

    Animals encounter microorganisms in their habitats, adapting physiology and behavior accordingly. The nematode Caenorhabditis elegans is found in microbe-rich environments; however, its responses to fungi are not extensively studied. Here, we describe interactions of C.elegans and Penicillium brevicompactum, an ecologically relevant mold. Transcriptome studies reveal that co-culture upregulates stress response genes, including xenobiotic-metabolizing enzymes (XMEs), in C.elegans intestine and AMsh glial cells. The nuclear hormone receptors (NHRs) NHR-45 and NHR-156 are induction regulators, and mutants that cannot induce XMEs in the intestine when exposed to P.brevicompactum experience mitochondrial stress and exhibit developmental defects. Different C.elegans wild isolates harbor sequence polymorphisms in nhr-156, resulting in phenotypic diversity in AMsh glia responses to microbe exposure. We propose that P.brevicompactum mitochondria-targeting mycotoxins are deactivated by intestinal detoxification, allowing tolerance to moldy environments. Our studies support the idea that C.elegans NHRs may be regulated by environmental cues.

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