Gene Expression and Regulation Section, Laboratory of Molecular and Cellular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892-0830, USA.
J Bacteriol. 2010 Nov;192(21):5580-7. doi: 10.1128/JB.00338-10. Epub 2010 Aug 20.
During infection of Escherichia coli, bacteriophage T4 usurps the host transcriptional machinery, redirecting it to the expression of early, middle, and late phage genes. Middle genes, whose expression begins about 1 min postinfection, are transcribed both from the extension of early RNA into middle genes and by the activation of T4 middle promoters. Middle-promoter activation requires the T4 transcriptional activator MotA and coactivator AsiA, which are known to interact with σ(70), the specificity subunit of RNA polymerase. T4 motA amber [motA(Am)] or asiA(Am) phage grows poorly in wild-type E. coli. However, previous work has found that T4 motA(Am)does not grow in the E. coli mutant strain TabG. We show here that the RNA polymerase in TabG contains two mutations within its β-subunit gene: rpoB(E835K) and rpoB(G1249D). We find that the G1249D mutation is responsible for restricting the growth of either T4 motA(Am)or asiA(Am) and for impairing transcription from MotA/AsiA-activated middle promoters in vivo. With one exception, transcription from tested T4 early promoters is either unaffected or, in some cases, even increases, and there is no significant growth phenotype for the rpoB(E835K G1249D) strain in the absence of T4 infection. In reported structures of thermophilic RNA polymerase, the G1249 residue is located immediately adjacent to a hydrophobic pocket, called the switch 3 loop. This loop is thought to aid in the separation of the RNA from the DNA-RNA hybrid as RNA enters the RNA exit channel. Our results suggest that the presence of MotA and AsiA may impair the function of this loop or that this portion of the β subunit may influence interactions among MotA, AsiA, and RNA polymerase.
在大肠杆菌感染过程中,噬菌体 T4 篡夺宿主转录机制,将其重新导向早期、中期和晚期噬菌体基因的表达。中期基因的表达始于感染后约 1 分钟,既可以通过早期 RNA 延伸到中期基因进行转录,也可以通过 T4 中期启动子的激活进行转录。T4 启动子激活需要 T4 转录激活因子 MotA 和共激活因子 AsiA,它们已知与 RNA 聚合酶的特异性亚基 σ(70)相互作用。T4 motA 琥珀突变体 [motA(Am)]或 asiA(Am)噬菌体在野生型大肠杆菌中生长不良。然而,之前的研究发现 T4 motA(Am)在大肠杆菌突变株 TabG 中不能生长。我们在这里表明,TabG 中的 RNA 聚合酶在其β亚基基因中存在两个突变:rpoB(E835K)和 rpoB(G1249D)。我们发现 G1249D 突变负责限制 T4 motA(Am)或 asiA(Am)的生长,并损害体内 MotA/AsiA 激活的中期启动子的转录。除一个例外,测试的 T4 早期启动子的转录要么不受影响,要么在某些情况下甚至增加,并且在没有 T4 感染的情况下,rpoB(E835K G1249D)菌株没有明显的生长表型。在报道的热稳定 RNA 聚合酶结构中,G1249 残基位于一个称为开关 3 环的疏水性口袋的正下方。该环被认为有助于 RNA 进入 RNA 出口通道时将 RNA 与 DNA-RNA 杂交体分离。我们的结果表明,MotA 和 AsiA 的存在可能会损害该环的功能,或者该β亚基的这一部分可能会影响 MotA、AsiA 和 RNA 聚合酶之间的相互作用。