Waksman Institute for Microbiology, 190 Frelinghuysen Road, Piscataway, NJ 08854, USA.
J Mol Biol. 2010 Sep 10;402(1):118-26. doi: 10.1016/j.jmb.2010.07.012. Epub 2010 Jul 19.
Bacteriophage T7 relies on its own RNA polymerase (RNAp) to transcribe its middle and late genes. Early genes, which include the viral RNAp gene, are transcribed by the host RNAp from three closely spaced strong promoters-A1, A2, and A3. One middle T7 gene product, gp2, is a strong inhibitor of the host RNAp. Gp2 is essential and is required late in infection, during phage DNA packaging. Here, we explore the role of gp2 in controlling host RNAp transcription during T7 infection. We demonstrate that in the absence of gp2, early viral transcripts continue to accumulate throughout the infection. Decreasing transcription from early promoter A3 is sufficient to make gp2 dispensable for phage infection. Gp2 also becomes dispensable when an antiterminating element boxA, located downstream of early promoters, is deleted. The results thus suggest that antiterminated transcription by host RNAp from the A3 promoter is interfering with phage development and that the only essential role for gp2 is to prevent this transcription.
噬菌体 T7 依赖其自身的 RNA 聚合酶（RNAp）来转录其中期和晚期基因。早期基因，包括病毒 RNAp 基因，由宿主 RNAp 从三个紧密间隔的强启动子 A1、A2 和 A3 转录。gp2 是一种中间 T7 基因产物，它是宿主 RNAp 的强烈抑制剂。gp2 是必需的，在感染后期，在噬菌体 DNA 包装过程中需要。在这里，我们探讨了 gp2 在控制 T7 感染过程中宿主 RNAp 转录的作用。我们证明，在没有 gp2 的情况下，早期病毒转录物在整个感染过程中继续积累。减少来自早期启动子 A3 的转录足以使 gp2 对噬菌体感染不再必需。当位于早期启动子下游的终止子盒 A 缺失时，gp2 也变得可有可无。因此，结果表明，宿主 RNAp 从 A3 启动子进行的抗终止转录干扰了噬菌体的发育，而 gp2 的唯一必需作用是防止这种转录。
