1
RIKEN Center for Developmental Biology and PRESTO, Japan Science and Technology Corporation, Chuo-ku, Kobe 650-0047, Japan.
2
Research Center for Glycoscience, National Institute of Advanced Industrial Science and Technology, AIST Central 6, Tsukuba 305-8566, Japan.
3
Department of Molecular Biology, Graduate school of Science, Institute for Advanced Research, Nagoya University, and CREST, Japan Science and Technology Corporation, Chikusa-ku, Nagoya 464-8602, Japan.
4
Department of Molecular and Medical Genetics, University of Toronto, Toronto, Ontario, Canada M5S 1A8.
In the nematode Caenorhabditis elegans, the gonad acquires two U-shaped arms through the directed migration of its distal tip cells (DTCs), which are located at the tip of the growing gonad arms1. A member of the ADAM (a disintegrin and metalloprotease) family, MIG-17, regulates directional migration of DTCs: MIG-17 is synthesized and secreted from the muscle cells of the body wall, and diffuses to the gonad where it is required for DTC migration2. The mig-23 mutation causes defective migration of DTCs and interacts genetically with mig-17. Here, we report that mig-23 encodes a membrane-bound nucleoside diphosphatase (NDPase) required for glycosylation and proper localization of MIG-17. Our findings indicate that an NDPase affects organ morphogenesis through glycosylation of the MIG-17 ADAM protease.
MORE ARTICLES LIKE THIS
These links to content published by NPG are automatically generated.
