ArticleCell death and differentiation2019
MiR-35 buffers apoptosis thresholds in the C. elegans germline by antagonizing both MAPK and core apoptosis pathways.
Article in Cell death and differentiation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 43 citations in OpenAlex.
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- Recent advances in understanding microRNA function and regulation in C. elegans.Seminars in cell & developmental biology · 2024Review
- Cerium oxide nanoparticles-carrying human umbilical cord mesenchymal stem cells counteract oxidative damage and facilitate tendon regeneration.Journal of nanobiotechnology · 2023Article
- Extracellular vesicle-transmitted miR-671-5p alleviates lung inflammation and injury by regulating the AAK1/NF-κB axis.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- A Compilation of the Diverse miRNA Functions inInternational journal of molecular sciences · 2023Review
- The developmentally timed decay of an essential microRNA family is seed-sequence dependent.Cell reports · 2022Article
- DNA repair, recombination, and damage signaling.Genetics · 2022Review
- Reproductive Toxicity of Furfural Acetone inCells · 2022Article
- Germ cell apoptosis is critical to maintain Caenorhabditis elegans offspring viability in stressful environments.PloS one · 2021Article
- Exploring the Molecular Mechanism of lncRNA-miRNA-mRNA Networks in Non-Syndromic Cleft Lip with or without Cleft Palate.International journal of general medicine · 2021Article
- Vorinostat-loaded titanium oxide nanoparticles (anatase) induce G2/M cell cycle arrest in breast cancer cells via3 Biotech · 2020Article
- In vivo CRISPR screening for phenotypic targets of theGenes & development · 2020Article
- NME/NM23/NDPK and Histidine Phosphorylation.International journal of molecular sciences · 2020Review
- The Function of NM23-H1/NME1 and Its Homologs in Major Processes Linked to Metastasis.Pathology oncology research : POR · 2020Review
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.