Barbé J, Villaverde A, Guerrero R
Antonie Van Leeuwenhoek. 1983 Nov;49(4-5):471-84. doi: 10.1007/BF00399325.
Infection of non-UV-irradiated cells of Salmonella typhimurium with UV-damaged P22 or KB1 phage induces recA-dependent inhibition of cell division, cell mutagenesis and prophage induction but not inhibition of respiration. On the contrary, respiration and ATP concentration are increased after treatment with UV-damaged phage in both RecA+ and RecA- strains, showing that this increase is not recA-dependent. Furthermore, infection with UV-damaged phage prevents both inhibition of respiration and decrease in ATP level in the UV-irradiated RecA+ strain. This indirect induction of SOS functions is related to degradation of phage DNA as well as to the multiplicity of infection used, suggesting that DNA degradation may play an important role in the mechanism of expression of the SOS system. Our results give also support to the hypothesis that there exists a differentiation in the expression of the various SOS functions.
用紫外线损伤的P22或KB1噬菌体感染未受紫外线照射的鼠伤寒沙门氏菌细胞,会诱导recA依赖性的细胞分裂抑制、细胞诱变和原噬菌体诱导,但不会抑制呼吸作用。相反,在RecA+和RecA-菌株中,用紫外线损伤的噬菌体处理后,呼吸作用和ATP浓度都会增加,这表明这种增加不依赖于recA。此外,用紫外线损伤的噬菌体感染可防止紫外线照射的RecA+菌株中呼吸作用的抑制和ATP水平的降低。这种SOS功能的间接诱导与噬菌体DNA的降解以及所用的感染复数有关,这表明DNA降解可能在SOS系统的表达机制中起重要作用。我们的结果也支持这样一种假设,即各种SOS功能的表达存在差异。