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Species » C. elegans(Genome assembly: WBcel235)

Expression cluster » WBPaper00060014:set-2(tm1630)_downregulated

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  • Overview

    WBPaper00060014:set-2(tm1630)_downregulated

    Species:
    Caenorhabditis elegans
    WormBase ID:
    WBPaper00060014:set-2(tm1630)_downregulated
    Transcripts that showed significantly decreased expression in set-2(tm1630) animals at embryo stage, comparing to in N2 animals.

    Algorithm:

    DESeq2 (v2.1.8.3) was used to determine DE genes and to generate principal component and scatter plots. DE genes with FDR < 0.05 were analysed using g:Profiler with Bonferroni correction.

    Remarks:
  • Associations

    Anatomy Terms:
    Life Stages:
    Life Stages Definition
    embryo CeThe whole period of embryogenesis in the nematode Caenorhabditis elegans, from the formation of an egg until hatching.
    GO terms:
    Processes:
  • References

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    • Journal article

      1

    1 reference found
    Regulators of H3K4 methylation mutated in neurodevelopmental disorders control axon guidance in <i>C. elegans</i>.
    Journal article
    Development
    2020

    Post-translational histone modifications regulate chromatin compaction and gene expression to control many aspects of development. Mutations in genes encoding regulators of H3K4 methylation are causally associated with neurodevelopmental disorders characterized by intellectual disability and deficits in motor functions. However, it remains unclear how H3K4 methylation influences nervous system development and contributes to the aetiology of disease. Here, we show that the catalytic activity of <i>set-2</i>, the <i>C. elegans</i> homolog of the H3K4 methyltransferase KMT2F/G (SETD1A/B) genes, controls embryonic transcription of neuronal genes and is required for establishing proper axon guidance and for neuronal functions related to locomotion and learning. Moreover, we uncover a striking correlation between components of the H3K4 regulatory machinery mutated in neurodevelopmental disorders and the process of axon guidance in <i>C. elegans</i> Thus, our study supports an epigenetic-based model for the aetiology of neurodevelopmental disorders, based on aberrant axon guidance process originating from deregulated H3K4 methylation.

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