Kaufmann G, David M, Borasio G D, Teichmann A, Paz A, Amitsur M
J Mol Biol. 1986 Mar 5;188(1):15-22. doi: 10.1016/0022-2836(86)90476-6.
Anticodon loop cleavages of two host tRNA species occur in bacteriophage T4-infected Escherichia coli CTr5X, a host strain restricting phage mutants deficient in polynucleotide kinase (pnk) or RNA ligase (rli). The cleavage products accumulate with the mutants but are further processed in wt infection through polynucleotide kinase and RNA ligase reactions. Inactivating mutations in stp suppress pnk- or rli- mutations in E. coli CTr5X and, as shown here, also abolish the anticodon nuclease, implicating the stp product with this activity. We show also that there exist other suppressing mutations of a pnk- (pseT2) mutation that appear not to affect the anticodon nuclease and are not in stp. It has been shown that a single locus in E. coli CTr5X, termed prr, determines the restriction of pnk- or rli- mutants. A transductant carrying prr featured upon infection the anticodon nuclease reaction products, suggesting that prr determines the specific manifestation of this activity. However, prr does not encode the tRNA species that are vulnerable to the anticodon nuclease.
在噬菌体T4感染的大肠杆菌CTr5X中，两种宿主tRNA物种的反密码子环发生切割，CTr5X是一种宿主菌株，可限制缺乏多核苷酸激酶（pnk）或RNA连接酶（rli）的噬菌体突变体。切割产物在突变体中积累，但在野生型感染中通过多核苷酸激酶和RNA连接酶反应进一步加工。stp中的失活突变抑制了大肠杆菌CTr5X中的pnk或rli突变，并且如本文所示，还消除了反密码子核酸酶，这表明stp产物具有这种活性。我们还表明，存在其他抑制pnk-（pseT2）突变的突变，这些突变似乎不影响反密码子核酸酶，且不在stp中。已经表明，大肠杆菌CTr5X中的一个单一基因座，称为prr，决定了对pnk或rli突变体的限制。携带prr的转导子在感染时具有反密码子核酸酶反应产物，这表明prr决定了这种活性的具体表现。然而，prr并不编码易受反密码子核酸酶作用的tRNA物种。
