Zengel J M, Lindahl L
J Bacteriol. 1985 Jul;163(1):140-7. doi: 10.1128/jb.163.1.140-147.1985.
In the 5 to 10 min immediately following a shift from 30 to 42 degrees C, the differential synthesis rates of ribosomal proteins encoded by the 11-gene S10 operon are transiently decreased. This effect results largely from a two- to threefold decrease in the differential rate of transcription of the operon. The inhibition of mRNA synthesis is apparently due to two types of control: (i) initiation of transcription at the S10 promoter is inhibited and (ii) readthrough at the attenuator in the S10 leader is decreased. Both of these effects on transcription are independent of the heat shock regulatory gene, htpR. Furthermore, the inhibition of transcription is observed in both relA+ and relA cells, suggesting that the temperature-induced repression does not require the relA-dependent accumulation of guanosine tetraphosphate (ppGpp). However, recovery from the heat shock was slower in relA+ strains than in relA strains. None of the other ribosomal protein operons that we analyzed showed such a strong decrease in transcription after the heat shock.
在从30摄氏度转变为42摄氏度后的5到10分钟内,由11个基因组成的S10操纵子编码的核糖体蛋白的差异合成速率会短暂下降。这种效应主要是由于该操纵子转录差异速率下降了两到三倍。mRNA合成的抑制显然是由于两种类型的控制:(i)S10启动子处的转录起始受到抑制,(ii)S10前导序列中衰减子处的通读减少。这两种对转录的影响均独立于热休克调节基因htpR。此外,在relA +和relA细胞中均观察到转录抑制,这表明温度诱导的阻遏不需要依赖relA的四磷酸鸟苷(ppGpp)积累。但是,relA +菌株从热休克中恢复的速度比relA菌株慢。我们分析的其他核糖体蛋白操纵子在热休克后均未显示出如此强烈的转录下降。