作者: Thomas H. Hohle , Mark R. O'Brian
DOI: 10.1111/MMI.12687
关键词: Mutant 、 Transporter 、 Biology 、 Intracellular 、 Manganese 、 Enzyme 、 Biochemistry 、 Bradyrhizobium japonicum 、 Extracellular 、 Magnesium 、 Molecular biology 、 Microbiology
摘要: A Bradyrhizobium japonicum mutant defective in the gene encoding high-affinity Mn(2+) transporter MntH has a severe growth phenotype under manganese limitation. Here, we isolated suppressor mutants of an mntH strain that grew limitation, and activities transport -dependent enzymes were partially rescued. The strains harbour gain-of-function mutations Mg(2+) channel MgtE. MgtE variants likely allow entry via loss gating mechanism normally holds closed state when cellular levels are high. Both MgtE-dependent MgtE-independent phenotypes recapitulated by magnesium-limited strain. Growth studies wild-type cells suggest is toxic to environmental magnesium low. Moreover, extracellular manipulated inhibit without substantially altering intracellular content either metal, implying toxicity depends on its distribution rather than absolute concentration. enzyme found be inhibited or stimulated . We conclude can occupy binding sites cells, processes targets toxicity.