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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Veröffentlicht in: | Cell reports (Cambridge) 2012-09, Vol.2 (3), p.526-539 |
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Sprache: | eng |
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Zusammenfassung: | 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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► Winner clones do not need draper, wasp, or psr to preserve growth advantage ► Winner cells do not need draper, wasp, or psr to kill loser cells ► Hemocytes are required for removal of the resulting apoptotic debris
Cell competition is a mechanism that removes viable but suboptimal cells from a growing population. It is believed that the genes wasp, psr, and draper are active in the cells that win the competition. Lolo, Tintó, and Moreno found that these genes are dispensable for cell-competition-induced apoptosis and winner cell overgrowth. Therefore, engulfment is a consequence—not a cause—of loser cells' death and is instead accomplished by recruited hemocytes. |
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ISSN: | 2211-1247 2211-1247 |
DOI: | 10.1016/j.celrep.2012.08.012 |