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W1430496411 startingPage "gkv923" @default.
W1430496411 abstract "Despite the fact that microRNAs (miRNAs) modulate the expression of around 60% of protein-coding genes, it is often hard to elucidate their precise role and target genes. Studying miRNA families as opposed to single miRNAs alone increases our chances of observing not only mutant phenotypes but also changes in the expression of target genes. Here we ask whether the TGF-β signalling pathways, which control many animal processes, might be modulated by miRNAs in Caenorhabditis elegans. Using a mutant for four members of the mir-58 family, we show that both TGF-β Sma/Mab (controlling body size) and TGF-β Dauer (regulating dauer, a stress-resistant larval stage) are upregulated. Thus, mir-58 family directly inhibits the expression of dbl-1 (ligand), daf-1, daf-4 and sma-6 (receptors) of TGF-β pathways. Epistasis experiments reveal that whereas the small body phenotype of the mir-58 family mutant must invoke unknown targets independent from TGF-β Sma/Mab, its dauer defectiveness can be rescued by DAF-1 depletion. Additionally, we found a negative feedback loop between TGF-β Sma/Mab and mir-58 and the related mir-80. Our results suggest that the interaction between mir-58 family and TGF-β genes is key on decisions about animal growth and stress resistance in C. elegans and perhaps other organisms." @default.
W1430496411 created "2016-06-24" @default.
W1430496411 creator A5006626895 @default.
W1430496411 creator A5056769047 @default.
W1430496411 creator A5059536224 @default.
W1430496411 date "2015-09-22" @default.
W1430496411 modified "2023-10-18" @default.
W1430496411 title "miR-58 family and TGF-β pathways regulate each other inCaenorhabditis elegans" @default.
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W1430496411 doi "https://doi.org/10.1093/nar/gkv923" @default.
W1430496411 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4783514" @default.
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