Journal
JOURNAL OF CELL BIOLOGY
Volume 212, Issue 1, Pages 39-49Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201510063
Keywords
-
Categories
Funding
- Agence Nationale de la Recherche [ANR-09-RPDOC-005-01]
- Fondation pour la Recherche Medicale [FRM-AJE201112]
- Mairie de Paris Emergence Program
- National Institutes of Health [NIH-R01-GM105775, NIH-R01-AG045842, NIH-DP2-OD008773]
Ask authors/readers for more resources
Cytokinesis, the physical division of one cell into two, is thought to be fundamentally similar in most animal cell divisions and driven by the constriction of a contractile ring positioned and controlled solely by the mitotic spindle. During asymmetric cell divisions, the core polarity machinery (partitioning defective [PAR] proteins) controls the unequal inheritance of key cell fate determinants. Here, we show that in asymmetrically dividing Caenorhabditis elegans embryos, the cortical PAR proteins (including the small guanosine triphosphatase CDC-42) have an active role in regulating recruitment of a critical component of the contractile ring, filamentous actin (F-actin). We found that the cortical PAR proteins are required for the retention of anillin and septin in the anterior pole, which are cytokinesis proteins that our genetic data suggest act as inhibitors of F-actin at the contractile ring. Collectively, our results suggest that the cortical PAR proteins coordinate the establishment of cell polarity with the physical process of cytokinesis during asymmetric cell division to ensure the fidelity of daughter cell formation.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available