| Summary: | A large-scale procedure was used to screen for deletions affecting growth of Saccharomyces cerevisiae when combined to ALG6 , ALG88, ALG10, CWH41, ROT2 or CNE1 deletions. 40 genes, grouped in 8 functional categories, were found to interact with the 6 query genes. The resulting network of 61 synthetic interactions was composed of 3 subnetworks, the N-glucosyltransferase (ALG6, ALG8, ALG10), the glucosidase (CWH41, ROT2) and CNE1 interaction sets, respectively. Deletion in 34 interacting genes conferred calcofluor white hypersensitivity, strengthening the relationship between N-glycan glucosylation/processing and cell wall physiology. In addition, a genetic interaction was found between ALG6 and SEC53, the yeast homologues of human ALG6 and PMM2 genes involved in congenital disorders of glycosylation. The alg6sec53 double mutant shows a synthetic growth defect and a CPY underglycosylation. Since this synthetic interaction is conserved from yeast to mammals, this work proposes the use of SGA analysis as a tool to uncover digenic effects that may underlie complex human genetic disorders.
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