2024-03-29T04:58:09Zhttp://repisalud.isciii.es/oai/requestoai:repisalud.isciii.es:20.500.12105/95262022-07-19T13:29:10Zcom_20.500.12105_2109com_20.500.12105_2052com_20.500.12105_2051col_20.500.12105_2110
00925njm 22002777a 4500
dc
de Lucas, Maria Pilar
author
Saez, Alberto G
author
Lozano, Encarnacion
author
2015-11-16
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.
Nucleic Acids Res. 2015 Nov 16;43(20):9978-93.
0305-1048
http://hdl.handle.net/20.500.12105/9526
26400166
10.1093/nar/gkv923
1362-4962
Nucleic acids research
miR-58 family and TGF-β pathways regulate each other in Caenorhabditis elegans