Hirochika H, Kobayashi Y
J Bacteriol. 1978 Dec;136(3):883-93.
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.
一类枯草芽孢杆菌的利福平抗性（rfm）突变可抑制耐夫西地酸突变体的温度敏感型芽孢形成。FUS426具有改变的延伸因子G。rfm突变仅抑制由延伸因子G突变引起的芽孢形成缺陷，但不能抑制其他类型的诱导芽孢形成缺陷。遗传和生化分析表明，rfm突变对芽孢形成的抑制是由RNA聚合酶中的单个突变引起的。在芽孢形成早期阶段后，通过将[3H]尿嘧啶或[3H]尿苷掺入RNA来测量，FUS426的RNA合成表观速率低于野生型菌株，并且这种降低通过rfm突变得以逆转。然而，当通过测量[3H]UTP和[3H]CTP的比活性来计算FUS426的RNA合成总速率时，它高于rfm突变体RIF122FUS426。本文讨论了芽孢形成过程中延伸因子G与RNA聚合酶之间功能相互作用的可能机制。
