進藤 麻子 (Howard Hughes Medical Institute and Section of Molecular Cell and Developmental Biology University of Texas, USA)

2011年09月28日(水) 16:00 より 17:30 まで

基礎生物学研究所　１階会議室 (111)

形態形成研究部門　上野 直人 (7570)

The Planar Cell Polarity (PCP) pathway is a critical regulator for cell behaviors during development, and convergent extension (CE) is an essential collective cell movement regulated by the PCP pathway. During this process, cells align and interdigitate to narrow and lengthen a tissue. PCP signaling is necessary for cell polarity during CE, but little is known about how PCP signaling controls the machinery that executes cell behaviors, for example actomyosin. Fritz is one of the PCP effector proteins that acts downstream of core PCP proteins (such as Dishevelled and Vangl2) to control specific processes in Drosophila. We show that vertebrate Fritz is necessary for CE and physically interacts with septins, cytoskeletal elements that provide cortical rigidity. Knockdown of Fritz or septin7 leads to abnormal cell membrane dynamics (rapid undulations) and defects in both cell shape and cell-cell contact. We have also found that Fritz controls septin7 and actin localization at the medio-lateral cell cortex. Fritz or septin7 KD disrupts polarized actin localization, and ectopic actin accumulation is observed instead. From these results, we conclude that polarized actin distribution is regulated by Fritz and septins downstream of PCP signaling to control membrane stability and cell shape during collective cell movement. 

※ セミナーは日本語で行います。