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First published online December 20, 2005

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New COGs in the organogenesis wheel

Congenital disorder of glycosylation (CDG) causes multiple developmental abnormalities in humans. To investigate the role of glycosylation and the Golgi (the principle site of glycosylation) in organogenesis, Nishiwaki and co-workers turned to the worm gonad. On p. 263, they report the cloning of two genes that, when mutated, cause worms to phenotypically resemble mig-17 mutants; mig-17 codes for an ADAM protease that is implicated in gonadal development. The two identified genes - cogc-1 and cogc-3 - encode homologues of members of the conserved oligomeric Golgi (COG) complex, which is involved in CDG, and in vesicle trafficking to, from and within the Golgi. Mutant analysis shows that these genes are needed for proper MIG-17 glycosylation and gonad formation, possibly together with other COG components. Although the mechanisms linking the COG complex to CDG are still unclear, the worm gonad should be a useful model for studying the roles of glycosylation in organogenesis.

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Related articles in Development:

The conserved oligomeric Golgi complex acts in organ morphogenesis via glycosylation of an ADAM protease in C. elegans

Yukihiko Kubota, Mitsue Sano, Saori Goda, Norio Suzuki, and Kiyoji Nishiwaki
Development 2006 133: 263-273. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in Development Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?