Abstract
A class of rifampin-resistant (rfm) mutations of Bacillus subtilis suppresses the temperature-sensitive sporulation of a fusidic acid-resistant mutant. FUS426, which has an altered elongation factor G. The rfm mutation suppressed only the sporulation defect caused by the elongation factor G mutation, but could not suppress other types of induced sporulation defects. Genetic and biochemical analyses showed that the sporulation suppression by the rfm mutation was caused by a single mutation in RNA polymerase. After the early sporulation phase, the apparent rate of RNA synthesis of FUS426, measured by [3H]uracil or [3H]uridine incorporation into RNA, became lower than that of the wild-type strain, and this decrease was reversed by the rfm mutation. However, when the total rate of RNA synthesis of FUS426 was calculated by measuring the specific activity of [3H]UTP and [3H]CTP, it was higher than that of the rfm mutant, RIF122FUS426. The possible mechanism of the functional interaction between elongation factor G and RNA polymerase during sporulation is discussed.
MeSH Terms
Bacillus subtilis/genetics,physiology
DNA-Directed RNA Polymerases/physiology
Genes
Mutation
Peptide Elongation Factors/physiology
RNA, Bacterial/biosynthesis
RNA, Ribosomal/biosynthesis
Spores, Bacterial
Temperature
Uridine Triphosphate/metabolism
Chemicals
Peptide Elongation Factors
RNA, Bacterial
RNA, Ribosomal
DNA-Directed RNA Polymerases
Uridine Triphosphate
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Hirochika H
Kobayashi Y
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