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Differential Gene expression of C. elegans larvae following tunicamycin treatment in the absence of manf-1

ABSTRACT: Microarray analysis was performed to evaluate the changes in gene expression that are associated with manf-1 deficiency with and without exposure to tunicamycin. RNA was isolated from four groups, (wildtype (N2) and manf-1 mutant (tm3603) L1 stage larve with and without 5 hours exposure to tunicmycin (5microgram/milliliter)) for transcriptomic profiles analysis

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE118294 | GEO | 2019/06/26

REPOSITORIES: GEO

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The neurotrophic factor MANF regulates autophagic flux and lysosome function to promote proteostasis in C. elegans

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Differential Gene expression of C. elegans larvae following tunicamycin treatment in the absence of manf-1

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Expression profile analysis of Drosophila melanogaster embryonic and larval MANF mutants together with paternal rescue and overexpression conditions

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MANF deletion abrogates early larval Caenorhabditis elegans stress response to tunicamycin and Pseudomonas aeruginosa.

Project description:Mesencephalic astrocyte-derived neurotrophic factor (MANF) is the only human neurotrophic factor with an evolutionarily-conserved C. elegans homolog, Y54G2A.23 or manf-1. MANF is a small, soluble, endoplasmic-reticulum (ER)-resident protein that is secreted upon ER stress and promotes survival of target cells such as neurons. However, the role of MANF in ER stress and its mechanism of cellular protection are not clear and the function of MANF in C. elegans is only beginning to emerge. In this study, we show that depletion of C. elegans manf-1 causes a slight decrease in lifespan and brood size; furthermore, combined depletion of manf-1 and the IRE-1/XBP-1 ER stress/UPR pathway resulted in sterile animals that did not produce viable progeny. We demonstrate upregulation of markers of ER stress in L1 larval nematodes, as measured by hsp-3 and hsp-4 transcription, upon depletion of manf-1 by RNAi or mutation; however, there was no difference in tunicamycin-induced expression of hsp-3 and hsp-4 between wild-type and MANF-deficient worms. Surprisingly, larval growth arrest observed in wild-type nematodes reared on tunicamycin is completely prevented in the manf-1 (tm3603) mutant. Transcriptional microarray analysis revealed that manf-1 mutant L1 larvae exhibit a novel modulation of innate immunity genes in response to tunicamycin. The hypothesis that manf-1 negatively regulates the innate immunity pathway is supported by our finding that the development of manf-1 mutant larvae compared to wild-type larvae is not inhibited by growth on P. aeruginosa. Together, our data represent the first characterization of C. elegans MANF as a key modulator of organismal ER stress and immunity.

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Expression profile analysis of Drosophila melanogaster embryonic and larval MANF mutants together with paternal rescue and overexpression conditions

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Gene expression profile in Liver of young and old mice with MANF overexpression

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