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Species » C. elegans(Genome assembly: WBcel235)

Expression cluster » WBPaper00056731:human-amylin_upregulated

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  • Overview

    WBPaper00056731:human-amylin_upregulated

    Species:
    Caenorhabditis elegans
    WormBase ID:
    WBPaper00056731:human-amylin_upregulated
    Transcripts that showed significantly increased expression in animals overexpression human amylin (driven by hsp-16.2).

    Algorithm:

    Differential gene expression analysiswas conducted using the DESeq R package (available from Bio-conductor). The DESeq analysis resulted in the determination of potential differentially expressed genes when compared between the DMH46 and N2 (wildtype) samples. The read counts for each sample were normalized for sequencing depth and distortion caused by highly differentially expressed genes.Then the negative bi nomial (NB) model was used to test the significance of differential expression between two genotypes.The differentially expressed genes were deemed significant if the FDR (False Discovery Rate) was less than 0.05, and the gene expression was above the 10th percentile, and showed greater than 2-fold change difference(overexpressed or underexpressed) between the conditions.

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  • Associations

    No associations data for WBPaper00056731:human-amylin_upregulated
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  • References

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      • Journal article

      1

    1 reference found
    An inducible model of human amylin overexpression reveals diverse transcriptional changes.
    Journal article
    Neurosci Lett
    2019

    Human Islet Amyloid Polypeptide or amylin is a neuroendocrine peptide with important endocrine and paracrine functions. Excessive production and accumulation of human amylin in the pancreas can lead to its aggregation and apoptosis of islet -cells. Amylin has been shown to function within the central nervous system to decrease food intake, and more recently, it has been revealed that amylin is directly transcribed from neurons of the central nervous system, including the hypothalamus, arcuate nucleus, medial preoptic area, and nucleus accumbens. These findings alter the current model of how amylin targets the nervous system, and as a result may lead to obesity and type II diabetes mellitus. Here we set out to use Caenorhabditis elegans as an inducible in vivo model system to study the effects of amylin overexpression in tissues that include the nervous system. We profiled the transcriptional changes in transgenic animals expressing human amylin through RNA-seq. Using this genome-wide approach our results revealed for the first time that expression of human amylin in tissues including the nervous system induce diverse physiological responses in various signaling pathways. From our characterization of transgenic C. elegans animals expressing human amylin, we also observed specific defects in neural developmental programs as well as sensory behavior. Taken together, our data demonstrate the utility of using C. elegans as a valuable in vivo model to study human amylin toxicity.

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  • Regulation

    Regulated by Gene:
    Iapp
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