Shankar Smita, Hatoum Asma, Roberts Jeffrey W
Department of Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853, USA.
Mol Cell. 2007 Sep 21;27(6):914-27. doi: 10.1016/j.molcel.2007.07.025.
The universal bacterial transcription elongation factor NusA mediates elongation activities of RNA polymerase. By itself, NusA induces transcription pausing and facilitates intrinsic termination, but NusA also is a cofactor of antiterminators that antagonize pausing and prevent termination. We show that NusA is required for lambda-related phage 82 antiterminator Q(82) to construct a stable complex in which RNA-based termination mechanisms have restricted access to the emerging transcript; this result suggests a locale for both Q(82) and NusA near the beta flap domain of RNA polymerase. Furthermore, as NusA is not required for the antipausing activity of Q(82) in vitro, we distinguish two distinct activities of antiterminators, namely antipausing and RNA occlusion, and discuss their roles in Q(82) function.
通用细菌转录延伸因子NusA介导RNA聚合酶的延伸活性。NusA自身可诱导转录暂停并促进内在终止,但它也是抗终止因子的辅因子,这些抗终止因子可对抗暂停并防止终止。我们发现,λ相关噬菌体82的抗终止因子Q(82)构建稳定复合物需要NusA,在该复合物中基于RNA的终止机制对新出现的转录本的访问受到限制;这一结果表明Q(82)和NusA在RNA聚合酶的β翼片结构域附近存在一个作用位点。此外,由于体外Q(82)的抗暂停活性不需要NusA,我们区分了抗终止因子的两种不同活性,即抗暂停和RNA封闭,并讨论了它们在Q(82)功能中的作用。