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

Author

Listed:
  • 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
    University of Toronto)

  • Mei Zhen

    (Lunenfeld-Tanenbaum Research Institute at Mount Sinai Hospital
    University of Toronto)

  • Anne-Claude Gingras

    (Lunenfeld-Tanenbaum Research Institute at Mount Sinai Hospital
    University of Toronto)

  • W Brent Derry

    (Developmental and Stem Cell Biology Program, The Hospital for Sick Children, Peter Gilgan Centre for Research and Learning
    University of Toronto)

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.

Suggested Citation

  • 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 & W Brent Derry, 2015. "CCM-3/STRIPAK promotes seamless tube extension through endocytic recycling," Nature Communications, Nature, vol. 6(1), pages 1-13, May.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7449
    DOI: 10.1038/ncomms7449
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