D'Ari R, George J, Huisman O
J Bacteriol. 1979 Nov;140(2):381-7. doi: 10.1128/jb.140.2.381-387.1979.
The tif-1 mutation in the Escherichia coli recA gene is known to cause induction of the various "SOS" functions at high temperature, including massive synthesis of the recA protein, lethal filamentation, elevated mutagenesis, and, in lambda lysogens, induction of prophage. It is shown here that the deoxyribonucleic acid initiation mutation dnaB252 suppresses all these manifestations of tif expression. Induction of lambda by ultraviolet irradiation, however, is not affected by the dnaB252 mutation. No similar suppression of tif is observed with other dnaB mutations affecting deoxyribonucleic acid elongation or with other deoxyribonucleic acid initiation mutations at the dnaA and dnaC loci. The fact that an alteration of the dnaB protein specifically suppresses tif-mediated SOS induction implies a role of the replication apparatus in this process, as has been suggested for ultraviolet induction. The induction of lambda is known to proceed via repressor cleavage, presumably promoted by an activated (protease) form of the recA protein. Since lambda induction is normal after ultraviolet irradiation of the tif-1 dnaB252(lambda) strain, tif-mediated induction in this strain may be blocked in a tif-specific step leading to activation of the recA (tif) protein. It is possible that the recA (tif) mutant protein may be directly involved in the replication complex in processes leading to this activation.
已知大肠杆菌recA基因中的tif-1突变会在高温下引发各种“SOS”功能的诱导，包括recA蛋白的大量合成、致死性丝状体形成、诱变率升高，以及在λ溶原菌中诱导原噬菌体。本文表明，脱氧核糖核酸起始突变dnaB252可抑制tif表达的所有这些表现。然而，紫外线照射诱导λ并不受dnaB252突变的影响。影响脱氧核糖核酸延伸的其他dnaB突变或dnaA和dnaC位点的其他脱氧核糖核酸起始突变均未观察到对tif的类似抑制作用。dnaB蛋白的改变特异性抑制tif介导的SOS诱导这一事实意味着复制装置在这一过程中发挥作用，正如紫外线诱导所表明的那样。已知λ的诱导是通过阻遏物裂解进行的，推测由recA蛋白的活化（蛋白酶）形式促进。由于tif-1 dnaB252(λ)菌株经紫外线照射后λ诱导正常，该菌株中tif介导的诱导可能在导致recA（tif）蛋白活化的tif特异性步骤中被阻断。有可能recA（tif）突变蛋白在导致这种活化的过程中直接参与复制复合体。
