METHYLAMINE-AMMONIA UPTAKE SYSTEMS IN SACCHAROMYCES-CEREVISIAE - MULTIPLICITY AND REGULATION

Three lines of evidence show that the uptake of methylamine/ammonia in Saccharomyces cerevisiae is mediated by at least two functionally distinct mechanisms. 1. Lineweaver-Burk plots for methylamine uptake show an abrupt transition between apparently linear sections, and both functions are inhibited competitively by ammonia. 2. These functions can be lost separately as a result of the two genetically unlinked mutations mep-1 and mep-2. Double (mep-1, mep-2) mutants grow very slowly in medium containing low concentrations of ammonia as sole nitrogen source, while both single mutants are little affected. Resistance to methylamine is linked to the mep-1 mutation which abolishes the high capacity metylamine uptake function. 3. both components of methylamine/ammonia uptake are subject to nitrogen catabolite repression. This control is relieved in a gdhCR mutant as well as in a gdhA-mutant. In a mutant with thermosensitive glutamine synthetase (glnts)grown on ammonia at 29°C, repression is lost for the high affinity component only, which indicates that glutamine is a necessary effector for the repression of only one of the components of the methylamine/ammonia transport mechanisms. This differential effect of the glntsmutation further supports the existence of the functionally distinct transport mechanisms. The npr-1 mutation seems to affect a pleiotrophic element involved either in the regulation or as a component of at least four uptake systems: the general aminoacid permease, the proline permease, the ureidosuccinic acid permease, and the high capacity methylamine/ammonia uptake function, all of which are strongly depressed in ammonia grown wild-type cells. Indications for a third ammonia uptake system were also obtained. © 1979 Springer-Verlag.