title: Manganese mutagenesis in yeast. VI. Mn2+ uptake, mitDNA replication and ER induction: comparison with other divalent cations.
abstract: A medium was found in which manganese efficiently induces erythromycin-resistant mitochondrial mutations, and which is suitable for measuring Mn2+ uptake and the labelling of DNA (fig. 1). Mn2+ uptake is stimulated by glucose and slowed down by cycloheximide (Fig 2). Mg2+ competes with Mn2+ uptake much stronger than does Zn2+ (Fig. 3). All of the conditions which favour Mn2+ uptake also favour induction of erythromycin-resistant mutations (Tables 3, 4). Mn2+ strongly inhibits protein synthesis (Table 1). Nuclear DNA replication is also strongly inhibited by this cation, while mitochondrial DNA replication is only weakly inhibited during the first 3 h of labelling, but there is small if any increase of the label incorporation between the 3rd 6th h of labelling (Table 2). The relation between label incorporation into mitDNA and mutation induction by manganese is not straightforward (Table 5). From among 11 divalent cations tested, only Mn2+ was capable of inducing mitochondrial erythromycin-resistant mutations (Table 6).
mesh_terms: D004261:DNA Replication; D004272:DNA, Mitochondrial / Q000096:biosynthesis*; D004352:Drug Resistance, Microbial; D004917:Erythromycin / Q000494:pharmacology; D008345:Manganese / Q000378:metabolism / Q000494:pharmacology*; D009153:Mutagens; D014176:Protein Biosynthesis; D012441:Saccharomyces cerevisiae / Q000187:drug effects / Q000378:metabolism*
chemical_list: D004272:DNA, Mitochondrial; D009153:Mutagens; D008345:Manganese; D004917:Erythromycin