CCM-3/STRIPAK promotes seamless tube extension through endocytic recycling

Benjamin Lant, Bin Yu, Marilyn Goudreault, Doug Holmyard, James D.R. Knight, Peter Xu, Linda Zhao, Kelly Chin, Evan Wallace, Mei Zhen, Anne-Claude Gingras and W Brent Derry ()
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Benjamin Lant: Developmental and Stem Cell Biology Program, The Hospital for Sick Children, Peter Gilgan Centre for Research and Learning
Bin Yu: Developmental and Stem Cell Biology Program, The Hospital for Sick Children, Peter Gilgan Centre for Research and Learning
Marilyn Goudreault: Lunenfeld-Tanenbaum Research Institute at Mount Sinai Hospital
Doug Holmyard: Lunenfeld-Tanenbaum Research Institute at Mount Sinai Hospital
James D.R. Knight: Lunenfeld-Tanenbaum Research Institute at Mount Sinai Hospital
Peter Xu: University of Toronto
Linda Zhao: Developmental and Stem Cell Biology Program, The Hospital for Sick Children, Peter Gilgan Centre for Research and Learning
Kelly Chin: Developmental and Stem Cell Biology Program, The Hospital for Sick Children, Peter Gilgan Centre for Research and Learning
Evan Wallace: Developmental and Stem Cell Biology Program, The Hospital for Sick Children, Peter Gilgan Centre for Research and Learning
Mei Zhen: Lunenfeld-Tanenbaum Research Institute at Mount Sinai Hospital
Anne-Claude Gingras: Lunenfeld-Tanenbaum Research Institute at Mount Sinai Hospital
W Brent Derry: Developmental and Stem Cell Biology Program, The Hospital for Sick Children, Peter Gilgan Centre for Research and Learning

Nature Communications, 2015, vol. 6, issue 1, 1-13

Abstract: Abstract The mechanisms governing apical membrane assembly during biological tube development are poorly understood. Here, we show that extension of the C. elegans excretory canal requires cerebral cavernous malformation 3 (CCM-3), independent of the CCM1 orthologue KRI-1. Loss of ccm-3 causes canal truncations and aggregations of canaliculular vesicles, which form ectopic lumen (cysts). We show that CCM-3 localizes to the apical membrane, and in cooperation with GCK-1 and STRIPAK, promotes CDC-42 signalling, Golgi stability and endocytic recycling. We propose that endocytic recycling is mediated through the CDC-42-binding kinase MRCK-1, which interacts physically with CCM-3–STRIPAK. We further show canal membrane integrity to be dependent on the exocyst complex and the actin cytoskeleton. This work reveals novel in vivo roles of CCM-3·STRIPAK in regulating tube extension and membrane integrity through small GTPase signalling and vesicle dynamics, which may help explain the severity of CCM3 mutations in patients.

Date: 2015
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DOI: 10.1038/ncomms7449

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