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 , 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.
