Hole-in-one mutant phenotypes link EGFR/ERK signaling to epithelial tissue repair in Drosophila.

<h4>Background</h4>Epithelia act as physical barriers protecting living organisms and their organs from the surrounding environment. Simple epithelial tissues have the capacity to efficiently repair wounds through a resealing mechanism. The known molecular mechanisms underlying this proc...

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Autores principales:	Jennifer A Geiger, Lara Carvalho, Isabel Campos, Ana Catarina Santos, Antonio Jacinto
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2011
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/aace2efc5cc547ee8933919b0be69d65
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spelling	oai:doaj.org-article:aace2efc5cc547ee8933919b0be69d652021-11-18T07:33:25ZHole-in-one mutant phenotypes link EGFR/ERK signaling to epithelial tissue repair in Drosophila.1932-620310.1371/journal.pone.0028349https://doaj.org/article/aace2efc5cc547ee8933919b0be69d652011-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22140578/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Epithelia act as physical barriers protecting living organisms and their organs from the surrounding environment. Simple epithelial tissues have the capacity to efficiently repair wounds through a resealing mechanism. The known molecular mechanisms underlying this process appear to be conserved in both vertebrates and invertebrates, namely the involvement of the transcription factors Grainy head (Grh) and Fos. In Drosophila, Grh and Fos lead to the activation of wound response genes required for epithelial repair. ERK is upstream of this pathway and known to be one of the first kinases to be activated upon wounding. However, it is still unclear how ERK activation contributes to a proper wound response and which molecular mechanisms regulate its activation.<h4>Methodology/principal findings</h4>In a previous screen, we isolated mutants with defects in wound healing. Here, we describe the role of one of these genes, hole-in-one (holn1), in the wound healing process. Holn1 is a GYF domain containing protein that we found to be required for the activation of several Grh and Fos regulated wound response genes at the wound site. We also provide evidence suggesting that Holn1 may be involved in the Ras/ERK signaling pathway, by acting downstream of ERK. Finally, we show that wound healing requires the function of EGFR and ERK signaling.<h4>Conclusions/significance</h4>Based on these data, we conclude that holn1 is a novel gene required for a proper wound healing response. We further propose and discuss a model whereby Holn1 acts downstream of EGFR and ERK signaling in the Grh/Fos mediated wound closure pathway.Jennifer A GeigerLara CarvalhoIsabel CamposAna Catarina SantosAntonio JacintoPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 11, p e28349 (2011)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Jennifer A Geiger Lara Carvalho Isabel Campos Ana Catarina Santos Antonio Jacinto Hole-in-one mutant phenotypes link EGFR/ERK signaling to epithelial tissue repair in Drosophila.
description	<h4>Background</h4>Epithelia act as physical barriers protecting living organisms and their organs from the surrounding environment. Simple epithelial tissues have the capacity to efficiently repair wounds through a resealing mechanism. The known molecular mechanisms underlying this process appear to be conserved in both vertebrates and invertebrates, namely the involvement of the transcription factors Grainy head (Grh) and Fos. In Drosophila, Grh and Fos lead to the activation of wound response genes required for epithelial repair. ERK is upstream of this pathway and known to be one of the first kinases to be activated upon wounding. However, it is still unclear how ERK activation contributes to a proper wound response and which molecular mechanisms regulate its activation.<h4>Methodology/principal findings</h4>In a previous screen, we isolated mutants with defects in wound healing. Here, we describe the role of one of these genes, hole-in-one (holn1), in the wound healing process. Holn1 is a GYF domain containing protein that we found to be required for the activation of several Grh and Fos regulated wound response genes at the wound site. We also provide evidence suggesting that Holn1 may be involved in the Ras/ERK signaling pathway, by acting downstream of ERK. Finally, we show that wound healing requires the function of EGFR and ERK signaling.<h4>Conclusions/significance</h4>Based on these data, we conclude that holn1 is a novel gene required for a proper wound healing response. We further propose and discuss a model whereby Holn1 acts downstream of EGFR and ERK signaling in the Grh/Fos mediated wound closure pathway.
format	article
author	Jennifer A Geiger Lara Carvalho Isabel Campos Ana Catarina Santos Antonio Jacinto
author_facet	Jennifer A Geiger Lara Carvalho Isabel Campos Ana Catarina Santos Antonio Jacinto
author_sort	Jennifer A Geiger
title	Hole-in-one mutant phenotypes link EGFR/ERK signaling to epithelial tissue repair in Drosophila.
title_short	Hole-in-one mutant phenotypes link EGFR/ERK signaling to epithelial tissue repair in Drosophila.
title_full	Hole-in-one mutant phenotypes link EGFR/ERK signaling to epithelial tissue repair in Drosophila.
title_fullStr	Hole-in-one mutant phenotypes link EGFR/ERK signaling to epithelial tissue repair in Drosophila.
title_full_unstemmed	Hole-in-one mutant phenotypes link EGFR/ERK signaling to epithelial tissue repair in Drosophila.
title_sort	hole-in-one mutant phenotypes link egfr/erk signaling to epithelial tissue repair in drosophila.
publisher	Public Library of Science (PLoS)
publishDate	2011
url	https://doaj.org/article/aace2efc5cc547ee8933919b0be69d65
work_keys_str_mv	AT jenniferageiger holeinonemutantphenotypeslinkegfrerksignalingtoepithelialtissuerepairindrosophila AT laracarvalho holeinonemutantphenotypeslinkegfrerksignalingtoepithelialtissuerepairindrosophila AT isabelcampos holeinonemutantphenotypeslinkegfrerksignalingtoepithelialtissuerepairindrosophila AT anacatarinasantos holeinonemutantphenotypeslinkegfrerksignalingtoepithelialtissuerepairindrosophila AT antoniojacinto holeinonemutantphenotypeslinkegfrerksignalingtoepithelialtissuerepairindrosophila
_version_	1718423307218321408

Hole-in-one mutant phenotypes link EGFR/ERK signaling to epithelial tissue repair in Drosophila.

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