Biology subjects

Chetluru, M.

Publications and source records attributed to Chetluru, M..

2 recordsLinked to original sources

bioRxiv2024

An essential mechanosensitive channel Pkd2 modulates the assembly of type II myosin and actin filaments in the cytokinetic contractile ring

Cytokinesis, the last step in cell division, separate daughter cells through the force produced by an actomyosin contractile ring assembled at the equatorial plane. In fission yeast cells, the ring helps recruit a mechanosensitive ion channel Pkd2 to the cleavage furrow, whose activation by membrane tension promotes calcium influx and daughter cell separation. However, it is unclear how the activities of Pkd2 may affect the actomyosin ring. Here, through both microscopic and genetic analyses of a hypomorphic mutant of the essential pkd2 gene, we examine its potential role in assembling and constricting the contractile ring. The pkd2-81KD mutation significantly increased the number of type II myosin heavy chain Myo2 (+20%), its regulatory light chain Rlc1 (+37%) and actin (+20%) molecules in the ring, compared to the wild type. Consistent with a regulatory role of Pkd2 in the ring assembly, we identified a strong negative genetic interaction between pkd2-81KD and the temperature-sensitive mutant myo2-E1. The pkd2-81KD myo2-E1 cells often failed to assemble a complete contractile ring. We conclude that Pkd2 modulates the recruitment of type II myosin and actin to the contractile ring, suggesting a novel calcium- dependent mechanism regulating the actin cytoskeletal structures during cytokinesis.

cell biology↗

bioRxiv2021

Fission yeast polycystin Pkd2p promotes transition to cell growth during cytokinesis

Polycystins are conserved mechanosensitive channels whose mutations lead to the common human renal disorder ADPKD. Previously we discovered that the plasma membrane-localized fission yeast homologue Pkd2p is an essential protein required for cytokinesis, but the mechanism remains unclear. Here, we isolated a novel temperature-sensitive mutant pkd2-B42. Among its strong growth defects, the most unique was that many mutant cells often lost significant portion of their volume in just 5 minutes followed by a gradual recovery, a process that we termed Deflation. Unlike cell lysis, deflation did not result in the plasma membrane rupture and it occurred independently from the cell cycle progression. The tip extension of pkd2-B42 cells was 80% slower than the wild type and their turgor pressure was 50% lower. Both pkd2-B42 and the other mutant pkd2-81KD partially rescued the mutants of the yeast Hippo signaling pathway Septation Initiation Network, by preventing cell lysis, enhancing septum formation, and doubling the number of Sid2/Mob1 molecules at the spindle pole bodies. We conclude that Pkd2p promotes cell size expansion during interphase by regulating turgor pressure and antagonizes SIN during cytokinesis. Summary statementMutations of polycystins lead to human genetic disorder ADPKD. We discovered that the fission yeast homologue Pkd2p promotes the cell expansion during interphase growth and antagonizes the Hippo pathway SIN during cytokinesis.

cell biology↗