Spire, an actin nucleation factor, regulates cell division during Drosophila heart development.

The Drosophila dorsal vessel is a beneficial model system for studying the regulation of early heart development. Spire (Spir), an actin-nucleation factor, regulates actin dynamics in many developmental processes, such as cell shape determination, intracellular transport, and locomotion. Through pro...

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Main Authors: Peng Xu, Tamara L Johnson, Jessica R Stoller-Conrad, Robert A Schulz
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2012-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC3262839?pdf=render
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spelling doaj-f83fbb48e39f4b5d86394bdb2c869fb42020-11-25T01:52:52ZengPublic Library of Science (PLoS)PLoS ONE1932-62032012-01-0171e3056510.1371/journal.pone.0030565Spire, an actin nucleation factor, regulates cell division during Drosophila heart development.Peng XuTamara L JohnsonJessica R Stoller-ConradRobert A SchulzThe Drosophila dorsal vessel is a beneficial model system for studying the regulation of early heart development. Spire (Spir), an actin-nucleation factor, regulates actin dynamics in many developmental processes, such as cell shape determination, intracellular transport, and locomotion. Through protein expression pattern analysis, we demonstrate that the absence of spir function affects cell division in Myocyte enhancer factor 2-, Tinman (Tin)-, Even-skipped- and Seven up (Svp)-positive heart cells. In addition, genetic interaction analysis shows that spir functionally interacts with Dorsocross, tin, and pannier to properly specify the cardiac fate. Furthermore, through visualization of double heterozygous embryos, we determines that spir cooperates with CycA for heart cell specification and division. Finally, when comparing the spir mutant phenotype with that of a CycA mutant, the results suggest that most Svp-positive progenitors in spir mutant embryos cannot undergo full cell division at cell cycle 15, and that Tin-positive progenitors are arrested at cell cycle 16 as double-nucleated cells. We conclude that Spir plays a crucial role in controlling dorsal vessel formation and has a function in cell division during heart tube morphogenesis.http://europepmc.org/articles/PMC3262839?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Peng Xu
Tamara L Johnson
Jessica R Stoller-Conrad
Robert A Schulz
spellingShingle Peng Xu
Tamara L Johnson
Jessica R Stoller-Conrad
Robert A Schulz
Spire, an actin nucleation factor, regulates cell division during Drosophila heart development.
PLoS ONE
author_facet Peng Xu
Tamara L Johnson
Jessica R Stoller-Conrad
Robert A Schulz
author_sort Peng Xu
title Spire, an actin nucleation factor, regulates cell division during Drosophila heart development.
title_short Spire, an actin nucleation factor, regulates cell division during Drosophila heart development.
title_full Spire, an actin nucleation factor, regulates cell division during Drosophila heart development.
title_fullStr Spire, an actin nucleation factor, regulates cell division during Drosophila heart development.
title_full_unstemmed Spire, an actin nucleation factor, regulates cell division during Drosophila heart development.
title_sort spire, an actin nucleation factor, regulates cell division during drosophila heart development.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2012-01-01
description The Drosophila dorsal vessel is a beneficial model system for studying the regulation of early heart development. Spire (Spir), an actin-nucleation factor, regulates actin dynamics in many developmental processes, such as cell shape determination, intracellular transport, and locomotion. Through protein expression pattern analysis, we demonstrate that the absence of spir function affects cell division in Myocyte enhancer factor 2-, Tinman (Tin)-, Even-skipped- and Seven up (Svp)-positive heart cells. In addition, genetic interaction analysis shows that spir functionally interacts with Dorsocross, tin, and pannier to properly specify the cardiac fate. Furthermore, through visualization of double heterozygous embryos, we determines that spir cooperates with CycA for heart cell specification and division. Finally, when comparing the spir mutant phenotype with that of a CycA mutant, the results suggest that most Svp-positive progenitors in spir mutant embryos cannot undergo full cell division at cell cycle 15, and that Tin-positive progenitors are arrested at cell cycle 16 as double-nucleated cells. We conclude that Spir plays a crucial role in controlling dorsal vessel formation and has a function in cell division during heart tube morphogenesis.
url http://europepmc.org/articles/PMC3262839?pdf=render
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AT tamaraljohnson spireanactinnucleationfactorregulatescelldivisionduringdrosophilaheartdevelopment
AT jessicarstollerconrad spireanactinnucleationfactorregulatescelldivisionduringdrosophilaheartdevelopment
AT robertaschulz spireanactinnucleationfactorregulatescelldivisionduringdrosophilaheartdevelopment
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