Cell Competition Time Line: Winners Kill Losers, which Are Extruded and Engulfed by Hemocytes
Cell competition is a mechanism that eliminates slow dividing cells from a growing population. It is believed that the genes wasp, psr, and draper are active in the cells that win the competition (“winner cells”) and that they are essential in the winner cells for the induction of apoptosis and for...
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2012-09-01
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Online Access: | http://www.sciencedirect.com/science/article/pii/S2211124712002379 |
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doaj-2a98337ff03947d781ff0be9829b966e2020-11-24T21:21:14ZengElsevierCell Reports2211-12472012-09-012352653910.1016/j.celrep.2012.08.012Cell Competition Time Line: Winners Kill Losers, which Are Extruded and Engulfed by HemocytesFidel-Nicolás Lolo0Sergio Casas-Tintó1Eduardo Moreno2Molecular Oncology Programme, Spanish National Cancer Centre (CNIO), Melchor Fernández Almagro 3, Madrid 28034, SpainMolecular Oncology Programme, Spanish National Cancer Centre (CNIO), Melchor Fernández Almagro 3, Madrid 28034, SpainInstitute of Cell Biology, University of Bern, Bern CH-3012, Switzerland Cell competition is a mechanism that eliminates slow dividing cells from a growing population. It is believed that the genes wasp, psr, and draper are active in the cells that win the competition (“winner cells”) and that they are essential in the winner cells for the induction of apoptosis and for the elimination of the “loser cells.” Here, we show that lack of those genes in winner cells appears to be dispensable for cell-competition-induced apoptosis and during dmyc-induced supercompetition. Moreover, winner clones do not need those genes in order to preserve their growth advantage. Finally, we find that most of the clearance of the apoptotic debris is not performed by winners but by recruited hemocytes, which are required for the removal of the apoptotic corpses at the very end. Therefore, engulfment is a consequence—not a cause—of loser cells' death. http://www.sciencedirect.com/science/article/pii/S2211124712002379 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Fidel-Nicolás Lolo Sergio Casas-Tintó Eduardo Moreno |
spellingShingle |
Fidel-Nicolás Lolo Sergio Casas-Tintó Eduardo Moreno Cell Competition Time Line: Winners Kill Losers, which Are Extruded and Engulfed by Hemocytes Cell Reports |
author_facet |
Fidel-Nicolás Lolo Sergio Casas-Tintó Eduardo Moreno |
author_sort |
Fidel-Nicolás Lolo |
title |
Cell Competition Time Line: Winners Kill Losers, which Are Extruded and Engulfed by Hemocytes |
title_short |
Cell Competition Time Line: Winners Kill Losers, which Are Extruded and Engulfed by Hemocytes |
title_full |
Cell Competition Time Line: Winners Kill Losers, which Are Extruded and Engulfed by Hemocytes |
title_fullStr |
Cell Competition Time Line: Winners Kill Losers, which Are Extruded and Engulfed by Hemocytes |
title_full_unstemmed |
Cell Competition Time Line: Winners Kill Losers, which Are Extruded and Engulfed by Hemocytes |
title_sort |
cell competition time line: winners kill losers, which are extruded and engulfed by hemocytes |
publisher |
Elsevier |
series |
Cell Reports |
issn |
2211-1247 |
publishDate |
2012-09-01 |
description |
Cell competition is a mechanism that eliminates slow dividing cells from a growing population. It is believed that the genes wasp, psr, and draper are active in the cells that win the competition (“winner cells”) and that they are essential in the winner cells for the induction of apoptosis and for the elimination of the “loser cells.” Here, we show that lack of those genes in winner cells appears to be dispensable for cell-competition-induced apoptosis and during dmyc-induced supercompetition. Moreover, winner clones do not need those genes in order to preserve their growth advantage. Finally, we find that most of the clearance of the apoptotic debris is not performed by winners but by recruited hemocytes, which are required for the removal of the apoptotic corpses at the very end. Therefore, engulfment is a consequence—not a cause—of loser cells' death.
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url |
http://www.sciencedirect.com/science/article/pii/S2211124712002379 |
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