Two different carriers transport both ammonium and methylammonium in Chlamydomonas reinhardtii.

A new methylammonium-resistant mutant strain from Chlamydomonas reinhardtii, henceforth termed 2172 (ma-2), has been isolated. This mutant is affected in a single mendelian gene different from and linked to the ma-1 locus which is defective in the methylammonium-resistant mutant 2170. Both mutations in ma-1 (2170) and ma-2 (2172) are linked to the nit-1 gene coding for the nitrate reductase apoenzyme. Mutant 2172 is affected in methylammonium but not in ammonium uptake capacity and shows derepressed nitrate and nitrite reductase activities in media containing nitrate plus methylammonium but not in nitrate plus ammonium media. The following two enzymatic components for the transport of both ammonium and methylammonium in wild-type cells have been identified: component 1, with high Vmax and K values, which is constitutive, and component 2, with low Vmax and K values, which is ammonium-repressible. Mutant 2170 lacks component 1 whereas mutant 2172 lacks component 2 for both methylammonium and ammonium transport. From genetic and kinetic evidences we conclude that in C. reinhardtii two different carriers are responsible for the transport of both ammonium and methylammonium and that methylammonium (ammonium) transport is a reversible process probably inhibited by the intracellular ammonium which, in turn, regulates nitrate and nitrite reductase levels.