Abstract
Polycystins are evolutionally conserved cation channels. Mutations of human polycystins lead to a common genetic disorder, Autosomal Dominant Polycystic Kidney Disorder. Interestingly, the fission yeast polycystin homologue Pkd2p is required for cytokinesis, the last stage of cell division, but the mechanism remains unclear. Motivated by our discovery of the epistatic genetic interactions between pkd2 and the Hippo pathway Septation Initiation Network (SIN), we investigated their interplay during cytokinesis. We found that pkd2 modulated the localization as well as the activities of SIN. Most notably, pkd2 promotes a transition to cell growth during cytokinesis, which is opposed by SIN. The role of Pkd2p in cell growth is not limited to cytokinesis. A newly isolated pkd2 temperature-sensitive mutant blocked the cell size expansion during interphase. Such growth defect was accompanied by frequent cell shrinking, reduced cell volume, and decreased cell stiffness. We conclude that Pkd2p promotes transition to the post-mitosis cell growth in coordination with the Hippo pathway.
Competing Interest Statement
The authors have declared no competing interest.
Abbreviations
- Septation initiation network
- (SIN)
- Spindle pole bodies
- (SPBs)
- Morphogenesis Orb6 related
- (MOR)