Polycystins are evolutionally conserved cation channels. Mutations of human polycystins lead to one of the most common genetic disorders, Autosomal Dominant Polycystic Kidney Disorder. Interestingly, the fission yeast 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 size growth during cytokinesis, opposed by SIN. The role of Pkd2p in cell growth is not limited to cytokinesis. A newly isolated pkd2 temperature-sensitive mutant largely blocked the tip expansion of cells during interphase. Such growth defect was accompanied by frequent 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
Staurosporine targets the Hippo pathway to inhibit cell growth
