Retallack D M, Johnson L L, Friedman D I
Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor 48109.
J Bacteriol. 1994 Apr;176(7):2082-9. doi: 10.1128/jb.176.7.2082-2089.1994.
Certain lambda-P22 hybrids, providing that they express the P22 C1 protein, fail to grow in Escherichia coli with the sipB391 mutation. We show that sipB391, previously located to the 57-min region of the E. coli chromosome, is a large deletion that extends into the 3' end of ssrA, a gene encoding the small stable 10Sa RNA. This deletion, apparently created by the excision of a cryptic prophage, CP4-57 (identified by Kirby et al. [J. E. Kirby, J. E. Trempy, and S. Gottesman, J. Bacteriol. 176:2068-2081]), leaves most of ssrA intact but removes the sequence encoding the 3' end of the precursor form of 10Sa RNA. The lack of functional 10Sa RNA, resulting from either the excision of CP4-57 or insertional inactivation of ssrA, appears to be responsible for the inhibition of lambda-P22 growth in E. coli with the sipB391 mutation. We propose that 10Sa RNA acts either directly or indirectly to facilitate removal of C1 protein from its DNA target site.
某些λ-P22杂种，只要它们表达P22 C1蛋白，就无法在带有sipB391突变的大肠杆菌中生长。我们发现，先前定位在大肠杆菌染色体57分钟区域的sipB391是一个大的缺失，它延伸到ssrA的3'端，ssrA是一个编码小稳定10Sa RNA的基因。这种缺失显然是由一个隐蔽原噬菌体CP4-57（由Kirby等人[J. E. Kirby, J. E. Trempy, and S. Gottesman, J. Bacteriol. 176:2068-2081]鉴定）的切除造成的，它使ssrA的大部分保持完整，但去除了编码10Sa RNA前体形式3'端的序列。由于CP4-57的切除或ssrA的插入失活导致缺乏功能性10Sa RNA，这似乎是导致带有sipB391突变的大肠杆菌中λ-P22生长受到抑制的原因。我们提出，10Sa RNA直接或间接地作用，以促进C1蛋白从其DNA靶位点的去除。
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