MiR-35 buffers apoptosis thresholds in the C. elegans germline by antagonizing both MAPK and core apoptosis pathways. View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2019-04-05

AUTHORS

Anh T Tran, Eric M Chapman, Mathieu N Flamand, Bin Yu, Samuel J Krempel, Thomas F Duchaine, Matthew Eroglu, W Brent Derry

ABSTRACT

Apoptosis is a genetically programmed cell death process with profound roles in development and disease. MicroRNAs modulate the expression of many proteins and are often deregulated in human diseases, such as cancer. C. elegans germ cells undergo apoptosis in response to genotoxic stress by the combined activities of the core apoptosis and MAPK pathways, but how their signalling thresholds are buffered is an open question. Here we show mir-35-42 miRNA family play a dual role in antagonizing both NDK-1, a positive regulator of MAPK signalling, and the BH3-only pro-apoptotic protein EGL-1 to regulate the magnitude of DNA damage-induced apoptosis in the C. elegans germline. We show that while miR-35 represses EGL-1 by promoting transcript degradation, repression of NDK-1 may be through sequestration of the transcript to inhibit translation. Importantly, dramatic increase in NDK-1 expression was observed in cells about to die. In the absence of miR-35, increased NDK-1 activity enhanced MAPK signalling that lead to significant increases in germ cell death. Our findings demonstrate that NDK-1 acts upstream of (or in parallel to) EGL-1, and that miR-35 targets both egl-1 and ndk-1 to fine-tune cell killing in response to genotoxic stress. More... »

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41418-019-0325-6

DOI

http://dx.doi.org/10.1038/s41418-019-0325-6

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1113261629

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30952991


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