Ionic remediability of a mutational transport defect in Chlamydomonas.

or quinolinic acid (or both). The modifying gene has no demonstrable effect on the utilization of exogenously supplied nicotinamide (K. Nakamura and C. S. Gowans, Genetics 51:931, 1965). Two observations strongly indicate that the modifying gene does not operate through a modification of the pathway of synthesis of niacin. First, the nicotinamide auxotrophs carrying the modifying gene grow normally on media supplemented with nicotinamide, even though it appears, in a variety of organisms, that nicotinamide is first deamidated to nicotinic acid before its utilization in the synthesis of nicotinamide adenine dinucleotide (J. Preiss and P. Handler, J. Biol. Chem. 233:493, 1958). Second, strains carrying mod-i alone (no nicotinamide-auxotrophic genes) grow normally on minimal medium, and therefore are utilizing endogenously synthesized quinolinic and nicotinic acids. It is thus most likely that the modifying gene exerts its effect on a transport mechanism involving nicotinic and quinolinic acids. Two mutant strains were utilized in these experiments: (i) Mo 11, which carries the nic-6 nicotinamide-auxotrophic gene and the mod-i modifying gene, and which therefore grows on