a raccdc-42–independent gitpixpak signaling pathway mediates cell migration in c. elegans一个raccdc-42-independent gitpixpak信号通路介导细胞迁移在秀丽隐杆线虫.pdfVIP
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a raccdc-42–independent gitpixpak signaling pathway mediates cell migration in c. elegans一个raccdc-42-independent gitpixpak信号通路介导细胞迁移在秀丽隐杆线虫
A RAC/CDC-42–Independent GIT/PIX/PAK Signaling
Pathway Mediates Cell Migration in C. elegans
Mark Lucanic1,2, Hwai-Jong Cheng1,2,3,4*
1 Center for Neuroscience, University of California Davis, Davis, California, United States of America, 2 Cell and Developmental Biology Graduate Group, University of
California Davis, Davis, California, United States of America, 3 Department of Neurobiology, Physiology and Behavior, College of Biological Sciences, University of California
Davis, Davis, California, United States of America, 4 Department of Pathology and Laboratory Medicine, School of Medicine, University of California Davis, Davis, California,
United States of America
Abstract
P21 activated kinase (PAK), PAK interacting exchange factor (PIX), and G protein coupled receptor kinase interactor (GIT)
compose a highly conserved signaling module controlling cell migrations, immune system signaling, and the formation of
the mammalian nervous system. Traditionally, this signaling module is thought to facilitate the function of RAC and CDC-42
GTPases by allowing for the recruitment of a GTPase effector (PAK), a GTPase activator (PIX), and a scaffolding protein (GIT)
as a regulated signaling unit to specific subcellular locations. Instead, we report here that this signaling module functions
independently of RAC/CDC-42 GTPases in vivo to control the cell shape and migration of the distal tip cells (DTCs) during
morphogenesis of the Caenorhabditis elegans gonad. In addition, this RAC/CDC-42–independent PAK pathway functions in
parallel to a classical GTPase/PAK pathway to control the guidance aspect of DTC migration. Among the C. elegans PAKs,
only PAK-1 functions in the GIT/PIX/PAK pathway independently of RAC/CDC42 GTPases, while both PAK-1 and MAX-2 are
redundantly utilized in the GTPase/PAK pathway. Both RAC/CDC42–dependent and –independent PAK pathways function
with the integrin recept
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