A role for N‐glycosylation in differential growth control and Drosophila development: phenotypic analysis of alg10

In this study we begin to phenotypically characterize Alg10, an enzyme that adds the terminal glucose residue to the growing dolichol‐linked oligosaccharide during N‐glycosylation prior to its en masse transfer to a nascent polypeptide. Genetic and molecular approaches were developed to characterize the alg10 loss of function phenotype during Drosophila development. While pleotrophic phenotypes were observed in alg10 mutant embryos, clonal analysis of the alg10 mutation in the developing wing yielded a smaller and rounder adult wing phenotype as compared to wild type. This implicates a potential link between glycosylation and pathways governing growth control. Both the Insulin receptor (InR) signaling pathway and the Epidermal growth factor pathway acting through c‐myc are known to control growth in Drosophila , roles that are conserved in mammals. To begin to address whether alg10 disrupts InR signaling, I examined the genetic interaction between alg10 and an activated form of InR that produced large disordered eyes. By removing half the Alg10 activity in this background, an enhanced phenotype was observed with an irregular eye surface, fused ommatidia, and patches of necrotic tissue. This indicates a genetic interaction between alg10 and the dInR pathway and suggests alg10 influences InR mediated growth control. This work was funded by an HHMI Undergraduate Research Fellowship.