Expression of LASS2 controlled by LAG1 or ADH1 promoters cannot functionally complement Lag1p

SummaryLAG1 contributes to the substrate specificity and catalytic activity of ceramide synthases in Saccharomyces cerevisiae. Double deletion of LAG1 and its yeast homologue LAC1 results in the slow growth defect of the cell under certain genetic backgrounds. LASS2, containing the conserved TLC domain and the specific HOX domain, is a human homologue of Lag1p. In this study, shuffling tests and tetrad analyses were carried out to examine the complementation between Lag1p and LASS2 or its fragment containing the TLC domain but lacking the HOX domain (LASS2ΔHOX). Controlled by either the natural weak LAG1 promoter or the strong yeast ADH1 promoter, LASS2 and LASS2ΔHOX could not rescue the slow growth defect of double mutant. The results indicated that LASS2 or LASS2ΔHOX could not functionally complement Lag1p.