

School Notes
Date posted: Oct 10, 2024
Marcus Harrell of the Das Lab won Best Poster at the 2024 Biology Department Retreat, voted by his peers and Biology Faculty members.
The abstract to Marcus' poster is included:
Title: The Cdc42 GEF, Scd1, localizes to cell ends via Diffusion to promote bipolar growth in S. pombe
Abstract: The Rho GTPase Cdc42 is highly conserved and a major regulator of polarized growth in most eukaryotes. In the bipolar yeast S. pombe, Cdc42 activity periodically oscillates between the two ends to promote growth. Both ends do not simultaneously remain active, and the active end must lose Cdc42 activation for the other end to gain Cdc42 activity. This suggests the two ends must compete for resources that activate Cdc42. However, the underlying mechanisms that coordinate the precise spatiotemporal activation of Cdc42 are not fully understood. One outstanding question is what resource do the two ends compete for? We previously found that disruption of branched actin (required for endocytosis) but not actin cables (required for exocytosis), impedes Scd1 localization (Cdc42 activator) which disrupts active Cdc42 dynamics. We further found that Scd1 localization was disrupted because endocytosis is required to remove the PAK kinase Pak1 (Scd1 inhibitor). These results suggest that Scd1 localization is essential for competition, but Scd1 is not directly localized by actin. Thus, we hypothesize that growing ends compete for Scd1 which diffuses between both ends. We tested this by quantifying the impact of increasing the mass of Scd1 on cell morphology and protein dynamics. We find that heavier Scd1 leads to more monopolar cells and slower Scd1 localization. Thus, we propose that the Cdc42 activator Scd1 diffuses along a concentration gradient between the two ends to promote periodic spatiotemporal activation of Cdc42.