Stewart Charles R, Yip Tameson K S, Myles Bati, Laughlin Laura
Department of Biochemistry and Cell Biology, Rice University, Houston, TX 77251, USA.
Virology. 2009 Sep 30;392(2):271-4. doi: 10.1016/j.virol.2009.06.046. Epub 2009 Aug 8.
A nonsense mutation in SPO1 gene 40 prevented normal shutoff of both host DNA and host RNA synthesis, showing that gp40 is required for the normal occurrence of both shutoffs. A gene 39 nonsense mutation caused accelerated shutoff of both host DNA and host RNA synthesis (aided by a gene 38 nonsense mutation), showing that gp39 (aided by gp38) limits the rate at which both shutoffs occur. The 40(-) mutation suppressed the accelerative effects of the 39(-) and 38(-) mutations, showing that gp40 also plays an essential role in the accelerated shutoffs. To the best of our knowledge, proteins with the particular activities implied for gp39 and gp40 have not been identified in any other bacteriophage. SPO1 has at least three different mechanisms that have the effect of delaying the shutoff of host DNA and RNA synthesis.
SPO1基因40中的无义突变阻止了宿主DNA和宿主RNA合成的正常关闭,表明gp40是这两种关闭过程正常发生所必需的。基因39无义突变导致宿主DNA和宿主RNA合成的加速关闭(在基因38无义突变的辅助下),表明gp39(在gp38的辅助下)限制了这两种关闭过程发生的速率。40(-)突变抑制了39(-)和38(-)突变的加速作用,表明gp40在加速关闭过程中也起着重要作用。据我们所知,在任何其他噬菌体中都未鉴定出具有gp39和gp40所暗示的特定活性的蛋白质。SPO1至少有三种不同的机制可延迟宿主DNA和RNA合成的关闭。