000126217 001__ 126217
000126217 005__ 20190316234327.0
000126217 0247_ $$2doi$$a10.1242/dev.019075
000126217 02470 $$2ISI$$a000254917500010
000126217 037__ $$aARTICLE
000126217 245__ $$aPLK-1 asymmetry contributes to asynchronous cell division of C. elegans embryos
000126217 269__ $$a2008
000126217 260__ $$c2008
000126217 336__ $$aJournal Articles
000126217 500__ $$aAuthor address: Swiss Institute for Experimental Cancer Research (ISREC Sciences, Swiss Federal Institute of Technology (EPFL), Lausanne, Switzerland
000126217 520__ $$aAcquisition of lineage-specific cell cycle duration is an important feature of metazoan development. In Caenorhabditis elegans, differences in cell cycle duration are already apparent in two-cell stage embryos, when the larger anterior blastomere AB divides before the smaller posterior blastomere P1. This time difference is under the control of anterior-posterior (A-P) polarity cues set by the PAR proteins. The mechanisms by which these cues regulate the cell cycle machinery differentially in AB and P1 are incompletely understood. Previous work established that retardation of P1 cell division is due in part to preferential activation of an ATL-1/CHK-1 dependent checkpoint in P1, but how the remaining time difference is controlled is not known. Here, we establish that differential timing relies also on a mechanism that promotes mitosis onset preferentially in AB. The polo-like kinase PLK-1, a positive regulator of mitotic entry, is distributed in an asymmetric manner in two-cell stage embryos, with more protein present in AB than in P1. We find that PLK-1 asymmetry is regulated by A-P polarity cues through preferential protein retention in the embryo anterior. Importantly, mild inactivation of plk-1 by RNAi delays entry into mitosis in P1, but not in AB, in a manner that is independent of ATL-1/CHK-1. Together, our findings support a model in which differential timing of mitotic entry in C. elegans embryos relies on two complementary mechanisms: ATL-1/CHK-1-dependent preferential retardation in P1 and PLK-1-dependent preferential promotion in AB, which together couple polarity cues and cell cycle progression during early development
000126217 6531_ $$aAnimals
000126217 6531_ $$aAnimals
000126217 6531_ $$aGenetically Modified
000126217 6531_ $$aCaenorhabditis elegans/cytology/embryology/physiology
000126217 6531_ $$aCell Cycle Proteins/metabolism
000126217 6531_ $$aCell Division
000126217 6531_ $$aCell Polarity/genetics
000126217 6531_ $$aEmbryo
000126217 6531_ $$aNonmammalian/cytology/metabolism
000126217 6531_ $$aMitosis/physiology
000126217 6531_ $$aModels
000126217 6531_ $$aBiological
000126217 6531_ $$aProtein-Serine-Threonine Kinases/metabolism
000126217 6531_ $$aProto-Oncogene Proteins/metabolism
000126217 6531_ $$aAnimals
000126217 700__ $$aBudirahardja, Yemima
000126217 700__ $$0243625$$aGönczy, Pierre$$g168676
000126217 773__ $$j135$$k7$$q1303-1313$$tDevelopment
000126217 8564_ $$zURL
000126217 8564_ $$s3636133$$uhttps://infoscience.epfl.ch/record/126217/files/Budirahardja%20%20Y_Development_2008.pdf$$zn/a
000126217 909C0 $$0252248$$pUPGON$$xU11155
000126217 909CO $$ooai:infoscience.tind.io:126217$$pSV$$particle$$qGLOBAL_SET
000126217 937__ $$aUPGON-ARTICLE-2008-008
000126217 973__ $$aEPFL$$rREVIEWED$$sPUBLISHED
000126217 980__ $$aARTICLE