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sta-1 is repressed by mir-58 family in Caenorhabditis elegans

The miR-58 family comprises 6 microRNAs with largely shared functions, and with an overall high expression, because one of its members, miR-58, is the most abundant microRNA in Caenorhabditis elegans. We recently found that 2 TGF-β signaling pathways, Sma/Mab and Dauer, responsible for body size and...

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Detalles Bibliográficos
Autores principales: Lozano, Encarnación, de Lucas, María Pilar, Sáez, Alberto G.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5190142/
https://www.ncbi.nlm.nih.gov/pubmed/28090395
http://dx.doi.org/10.1080/21624054.2016.1238560
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author Lozano, Encarnación
de Lucas, María Pilar
Sáez, Alberto G.
author_facet Lozano, Encarnación
de Lucas, María Pilar
Sáez, Alberto G.
author_sort Lozano, Encarnación
collection PubMed
description The miR-58 family comprises 6 microRNAs with largely shared functions, and with an overall high expression, because one of its members, miR-58, is the most abundant microRNA in Caenorhabditis elegans. We recently found that 2 TGF-β signaling pathways, Sma/Mab and Dauer, responsible for body size and dauer formation respectively, among other phenotypes, are downregulated by the miR-58 family. Here, we further explore this family by showing that it also acts through the sta-1 3′UTR. sta-1 encodes a transcription factor, homologous to mammalian STATs, that inhibits dauer formation in association with the TGF-β Dauer pathway. We also observe that mutants with a constitutively active TGF-β Dauer pathway express higher levels of sta-1 mRNA. Our results reinforce the view of the miR-58 family and STA-1 as regulators of dauer formation in coordination with the TGF-β Dauer pathway.
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spelling pubmed-51901422017-01-13 sta-1 is repressed by mir-58 family in Caenorhabditis elegans Lozano, Encarnación de Lucas, María Pilar Sáez, Alberto G. Worm Short Communication The miR-58 family comprises 6 microRNAs with largely shared functions, and with an overall high expression, because one of its members, miR-58, is the most abundant microRNA in Caenorhabditis elegans. We recently found that 2 TGF-β signaling pathways, Sma/Mab and Dauer, responsible for body size and dauer formation respectively, among other phenotypes, are downregulated by the miR-58 family. Here, we further explore this family by showing that it also acts through the sta-1 3′UTR. sta-1 encodes a transcription factor, homologous to mammalian STATs, that inhibits dauer formation in association with the TGF-β Dauer pathway. We also observe that mutants with a constitutively active TGF-β Dauer pathway express higher levels of sta-1 mRNA. Our results reinforce the view of the miR-58 family and STA-1 as regulators of dauer formation in coordination with the TGF-β Dauer pathway. Taylor & Francis 2016-09-21 /pmc/articles/PMC5190142/ /pubmed/28090395 http://dx.doi.org/10.1080/21624054.2016.1238560 Text en © 2016 The Author(s). Published with license by Taylor & Francis. http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.
spellingShingle Short Communication
Lozano, Encarnación
de Lucas, María Pilar
Sáez, Alberto G.
sta-1 is repressed by mir-58 family in Caenorhabditis elegans
title sta-1 is repressed by mir-58 family in Caenorhabditis elegans
title_full sta-1 is repressed by mir-58 family in Caenorhabditis elegans
title_fullStr sta-1 is repressed by mir-58 family in Caenorhabditis elegans
title_full_unstemmed sta-1 is repressed by mir-58 family in Caenorhabditis elegans
title_short sta-1 is repressed by mir-58 family in Caenorhabditis elegans
title_sort sta-1 is repressed by mir-58 family in caenorhabditis elegans
topic Short Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5190142/
https://www.ncbi.nlm.nih.gov/pubmed/28090395
http://dx.doi.org/10.1080/21624054.2016.1238560
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