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Repulsion by Slit and Roundabout prevents Shotgun/E-cadherin–mediated cell adhesion during Drosophila heart tube lumen formation
During Drosophila melanogaster heart development, a lumen forms between apical surfaces of contralateral cardioblasts (CBs). We show that Slit and its receptor Roundabout (Robo) are required at CB apical domains for lumen formation. Mislocalization of Slit outside the apical domain causes ectopic lu...
Autores principales: | , , , |
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Formato: | Texto |
Lenguaje: | English |
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The Rockefeller University Press
2008
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2483515/ https://www.ncbi.nlm.nih.gov/pubmed/18663139 http://dx.doi.org/10.1083/jcb.200804120 |
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author | Santiago-Martínez, Edgardo Soplop, Nadine H. Patel, Rajesh Kramer, Sunita G. |
author_facet | Santiago-Martínez, Edgardo Soplop, Nadine H. Patel, Rajesh Kramer, Sunita G. |
author_sort | Santiago-Martínez, Edgardo |
collection | PubMed |
description | During Drosophila melanogaster heart development, a lumen forms between apical surfaces of contralateral cardioblasts (CBs). We show that Slit and its receptor Roundabout (Robo) are required at CB apical domains for lumen formation. Mislocalization of Slit outside the apical domain causes ectopic lumen formation and the mislocalization of cell junction proteins, E-cadherin (E-Cad) and Enabled, without disrupting overall CB cell polarity. Ectopic lumen formation is suppressed in robo mutants, which indicates robo's requirement for this process. Genetic evidence suggests that Robo and Shotgun (Shg)/E-Cad function together in modulating CB adhesion. robo and shg/E-Cad transheterozygotes have lumen defects. In robo loss-of-function or shg/E-Cad gain-of-function embryos, lumen formation is blocked because of inappropriate CB adhesion and an accumulation of E-Cad at the apical membrane. In contrast, shg/E-Cad loss-of-function or robo gain-of-function blocks lumen formation due to a loss of CB adhesion. Our data show that Slit and Robo pathways function in lumen formation as a repulsive signal to antagonize E-Cad–mediated cell adhesion. |
format | Text |
id | pubmed-2483515 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2008 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-24835152009-01-28 Repulsion by Slit and Roundabout prevents Shotgun/E-cadherin–mediated cell adhesion during Drosophila heart tube lumen formation Santiago-Martínez, Edgardo Soplop, Nadine H. Patel, Rajesh Kramer, Sunita G. J Cell Biol Research Articles During Drosophila melanogaster heart development, a lumen forms between apical surfaces of contralateral cardioblasts (CBs). We show that Slit and its receptor Roundabout (Robo) are required at CB apical domains for lumen formation. Mislocalization of Slit outside the apical domain causes ectopic lumen formation and the mislocalization of cell junction proteins, E-cadherin (E-Cad) and Enabled, without disrupting overall CB cell polarity. Ectopic lumen formation is suppressed in robo mutants, which indicates robo's requirement for this process. Genetic evidence suggests that Robo and Shotgun (Shg)/E-Cad function together in modulating CB adhesion. robo and shg/E-Cad transheterozygotes have lumen defects. In robo loss-of-function or shg/E-Cad gain-of-function embryos, lumen formation is blocked because of inappropriate CB adhesion and an accumulation of E-Cad at the apical membrane. In contrast, shg/E-Cad loss-of-function or robo gain-of-function blocks lumen formation due to a loss of CB adhesion. Our data show that Slit and Robo pathways function in lumen formation as a repulsive signal to antagonize E-Cad–mediated cell adhesion. The Rockefeller University Press 2008-07-28 /pmc/articles/PMC2483515/ /pubmed/18663139 http://dx.doi.org/10.1083/jcb.200804120 Text en © 2008 Santiago-Martínez et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jcb.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/). |
spellingShingle | Research Articles Santiago-Martínez, Edgardo Soplop, Nadine H. Patel, Rajesh Kramer, Sunita G. Repulsion by Slit and Roundabout prevents Shotgun/E-cadherin–mediated cell adhesion during Drosophila heart tube lumen formation |
title | Repulsion by Slit and Roundabout prevents Shotgun/E-cadherin–mediated cell adhesion during Drosophila heart tube lumen formation |
title_full | Repulsion by Slit and Roundabout prevents Shotgun/E-cadherin–mediated cell adhesion during Drosophila heart tube lumen formation |
title_fullStr | Repulsion by Slit and Roundabout prevents Shotgun/E-cadherin–mediated cell adhesion during Drosophila heart tube lumen formation |
title_full_unstemmed | Repulsion by Slit and Roundabout prevents Shotgun/E-cadherin–mediated cell adhesion during Drosophila heart tube lumen formation |
title_short | Repulsion by Slit and Roundabout prevents Shotgun/E-cadherin–mediated cell adhesion during Drosophila heart tube lumen formation |
title_sort | repulsion by slit and roundabout prevents shotgun/e-cadherin–mediated cell adhesion during drosophila heart tube lumen formation |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2483515/ https://www.ncbi.nlm.nih.gov/pubmed/18663139 http://dx.doi.org/10.1083/jcb.200804120 |
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