ISL1 directly regulates FGF10 transcription during human cardiac outflow formation.

The LIM homeodomain gene Islet-1 (ISL1) encodes a transcription factor that has been associated with the multipotency of human cardiac progenitors, and in mice enables the correct deployment of second heart field (SHF) cells to become the myocardium of atria, right ventricle and outflow tract. Other...

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Autores principales:	Christelle Golzio, Emmanuelle Havis, Philippe Daubas, Gregory Nuel, Candice Babarit, Arnold Munnich, Michel Vekemans, Stéphane Zaffran, Stanislas Lyonnet, Heather C Etchevers
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/5b843ab15271402781cb5edc27449063
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spelling	oai:doaj.org-article:5b843ab15271402781cb5edc274490632021-11-18T07:29:10ZISL1 directly regulates FGF10 transcription during human cardiac outflow formation.1932-620310.1371/journal.pone.0030677https://doaj.org/article/5b843ab15271402781cb5edc274490632012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22303449/?tool=EBIhttps://doaj.org/toc/1932-6203The LIM homeodomain gene Islet-1 (ISL1) encodes a transcription factor that has been associated with the multipotency of human cardiac progenitors, and in mice enables the correct deployment of second heart field (SHF) cells to become the myocardium of atria, right ventricle and outflow tract. Other markers have been identified that characterize subdomains of the SHF, such as the fibroblast growth factor Fgf10 in its anterior region. While functional evidence of its essential contribution has been demonstrated in many vertebrate species, SHF expression of Isl1 has been shown in only some models. We examined the relationship between human ISL1 and FGF10 within the embryonic time window during which the linear heart tube remodels into four chambers. ISL1 transcription demarcated an anatomical region supporting the conserved existence of a SHF in humans, and transcription factors of the GATA family were co-expressed therein. In conjunction, we identified a novel enhancer containing a highly conserved ISL1 consensus binding site within the FGF10 first intron. ChIP and EMSA demonstrated its direct occupation by ISL1. Transcription mediated by ISL1 from this FGF10 intronic element was enhanced by the presence of GATA4 and TBX20 cardiac transcription factors. Finally, transgenic mice confirmed that endogenous factors bound the human FGF10 intronic enhancer to drive reporter expression in the developing cardiac outflow tract. These findings highlight the interest of examining developmental regulatory networks directly in human tissues, when possible, to assess candidate non-coding regions that may be responsible for congenital malformations.Christelle GolzioEmmanuelle HavisPhilippe DaubasGregory NuelCandice BabaritArnold MunnichMichel VekemansStéphane ZaffranStanislas LyonnetHeather C EtcheversPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 1, p e30677 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Christelle Golzio Emmanuelle Havis Philippe Daubas Gregory Nuel Candice Babarit Arnold Munnich Michel Vekemans Stéphane Zaffran Stanislas Lyonnet Heather C Etchevers ISL1 directly regulates FGF10 transcription during human cardiac outflow formation.
description	The LIM homeodomain gene Islet-1 (ISL1) encodes a transcription factor that has been associated with the multipotency of human cardiac progenitors, and in mice enables the correct deployment of second heart field (SHF) cells to become the myocardium of atria, right ventricle and outflow tract. Other markers have been identified that characterize subdomains of the SHF, such as the fibroblast growth factor Fgf10 in its anterior region. While functional evidence of its essential contribution has been demonstrated in many vertebrate species, SHF expression of Isl1 has been shown in only some models. We examined the relationship between human ISL1 and FGF10 within the embryonic time window during which the linear heart tube remodels into four chambers. ISL1 transcription demarcated an anatomical region supporting the conserved existence of a SHF in humans, and transcription factors of the GATA family were co-expressed therein. In conjunction, we identified a novel enhancer containing a highly conserved ISL1 consensus binding site within the FGF10 first intron. ChIP and EMSA demonstrated its direct occupation by ISL1. Transcription mediated by ISL1 from this FGF10 intronic element was enhanced by the presence of GATA4 and TBX20 cardiac transcription factors. Finally, transgenic mice confirmed that endogenous factors bound the human FGF10 intronic enhancer to drive reporter expression in the developing cardiac outflow tract. These findings highlight the interest of examining developmental regulatory networks directly in human tissues, when possible, to assess candidate non-coding regions that may be responsible for congenital malformations.
format	article
author	Christelle Golzio Emmanuelle Havis Philippe Daubas Gregory Nuel Candice Babarit Arnold Munnich Michel Vekemans Stéphane Zaffran Stanislas Lyonnet Heather C Etchevers
author_facet	Christelle Golzio Emmanuelle Havis Philippe Daubas Gregory Nuel Candice Babarit Arnold Munnich Michel Vekemans Stéphane Zaffran Stanislas Lyonnet Heather C Etchevers
author_sort	Christelle Golzio
title	ISL1 directly regulates FGF10 transcription during human cardiac outflow formation.
title_short	ISL1 directly regulates FGF10 transcription during human cardiac outflow formation.
title_full	ISL1 directly regulates FGF10 transcription during human cardiac outflow formation.
title_fullStr	ISL1 directly regulates FGF10 transcription during human cardiac outflow formation.
title_full_unstemmed	ISL1 directly regulates FGF10 transcription during human cardiac outflow formation.
title_sort	isl1 directly regulates fgf10 transcription during human cardiac outflow formation.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/5b843ab15271402781cb5edc27449063
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_version_	1718423409633787904

ISL1 directly regulates FGF10 transcription during human cardiac outflow formation.

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