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The core and conserved role of MAL is homeostatic regulation of actin levels
The transcription cofactor MAL is regulated by free actin levels and thus by actin dynamics. MAL, together with its DNA-binding partner, SRF, is required for invasive cell migration and in experimental metastasis. Although MAL/SRF has many targets, we provide genetic evidence in both Drosophila and...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Cold Spring Harbor Laboratory Press
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4035534/ https://www.ncbi.nlm.nih.gov/pubmed/24831700 http://dx.doi.org/10.1101/gad.237743.114 |
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author | Salvany, Lara Muller, Julius Guccione, Ernesto Rørth, Pernille |
author_facet | Salvany, Lara Muller, Julius Guccione, Ernesto Rørth, Pernille |
author_sort | Salvany, Lara |
collection | PubMed |
description | The transcription cofactor MAL is regulated by free actin levels and thus by actin dynamics. MAL, together with its DNA-binding partner, SRF, is required for invasive cell migration and in experimental metastasis. Although MAL/SRF has many targets, we provide genetic evidence in both Drosophila and human cellular models that actin is the key target that must be regulated by MAL/SRF for invasive cell migration. By regulating MAL/SRF activity, actin protein feeds back on production of actin mRNA to ensure sufficient supply of actin. This constitutes a dedicated homeostatic feedback system that provides a foundation for cellular actin dynamics. |
format | Online Article Text |
id | pubmed-4035534 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Cold Spring Harbor Laboratory Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-40355342014-11-15 The core and conserved role of MAL is homeostatic regulation of actin levels Salvany, Lara Muller, Julius Guccione, Ernesto Rørth, Pernille Genes Dev Research Communication The transcription cofactor MAL is regulated by free actin levels and thus by actin dynamics. MAL, together with its DNA-binding partner, SRF, is required for invasive cell migration and in experimental metastasis. Although MAL/SRF has many targets, we provide genetic evidence in both Drosophila and human cellular models that actin is the key target that must be regulated by MAL/SRF for invasive cell migration. By regulating MAL/SRF activity, actin protein feeds back on production of actin mRNA to ensure sufficient supply of actin. This constitutes a dedicated homeostatic feedback system that provides a foundation for cellular actin dynamics. Cold Spring Harbor Laboratory Press 2014-05-15 /pmc/articles/PMC4035534/ /pubmed/24831700 http://dx.doi.org/10.1101/gad.237743.114 Text en © 2014 Salvany et al.; Published by Cold Spring Harbor Laboratory Press http://creativecommons.org/licenses/by-nc/4.0/ This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/. |
spellingShingle | Research Communication Salvany, Lara Muller, Julius Guccione, Ernesto Rørth, Pernille The core and conserved role of MAL is homeostatic regulation of actin levels |
title | The core and conserved role of MAL is homeostatic regulation of actin levels |
title_full | The core and conserved role of MAL is homeostatic regulation of actin levels |
title_fullStr | The core and conserved role of MAL is homeostatic regulation of actin levels |
title_full_unstemmed | The core and conserved role of MAL is homeostatic regulation of actin levels |
title_short | The core and conserved role of MAL is homeostatic regulation of actin levels |
title_sort | core and conserved role of mal is homeostatic regulation of actin levels |
topic | Research Communication |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4035534/ https://www.ncbi.nlm.nih.gov/pubmed/24831700 http://dx.doi.org/10.1101/gad.237743.114 |
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