Involvement of other bacteriophage T4 genes in the blockade of protein synthesis and mRNA destabilization by a mutation of gene 61. 5.
Involvement of other bacteriophage T4 genes in the blockade of protein synthesis and mRNA destabilization by a mutation of gene 61. 5.
复制标题
其他噬菌体 T4 基因通过基因 61 突变参与蛋白质合成阻断和 mRNA 不稳定。 5.
作者：
T. Kai;H. Ueno;T. Yonesaki
噬菌体T4的基因61.5是感染后期基因表达所必需的；基因 61.5 的突变体显示晚期蛋白质的合成率降低，并在 30°C 感染不允许的宿主细胞时积累短转录本（T. Kai, H. E. Sellick, 和 T. Yonesaki, Genetics 144, 7-14, 1996）。在此我们描述，虽然缺陷仅在晚期才明显，但基因61.5在感染后早期表达，并且对功能性基因61.5的需求通过高温感染的早期和中期阶段的通过而得到部分补偿，这表明在早期和中期表达的T4基因绕过了高温下对基因61.5的需求。此外，我们分离了基因 61.5 突变体的 5 个假回复体，命名为 ssf1 至 ssf5，它们部分恢复了低温下的生长能力，稳定了 mRNA，并刺激了后期的蛋白质合成。这些结果强烈表明，在 T4 感染后期，其他 T4 基因的产物与基因 61.5 的产物相互作用，稳定了 mRNA。
Gene 61.5 of bacteriophage T4 is required for gene expression at late stages of infection; a mutant of gene 61.5 shows a reduced rate of synthesis of late proteins and accumulates short transcripts upon infection of nonpermissive host cells at 30 degreesC (T. Kai, H. E. Sellick, and T. Yonesaki, Genetics 144, 7-14, 1996). Here we describe that, although the defects are only apparent at late stages, gene 61.5 is expressed early after infection and that the requirement of a functional gene 61.5 is partially compensated by the passage of early and middle stages of infection at high temperatures, suggesting that T4 genes expressed at early and middle stages bypass the requirement for the gene 61.5 at high temperatures. Furthermore, we isolated five pseudorevertants of a gene 61.5 mutant, designated as ssf1 through ssf5, which partially restored the growth ability at low temperatures, stabilized mRNAs, and stimulated protein synthesis at late stages. These results strongly suggest that the products of other T4 genes interact with the product of gene 61.5 in stabilizing mRNAs late in T4 infection.
噬菌体 T4 的复制 DNA 解旋酶参与 DNA 重组。
影响因子：
3.3
作者：
Yonesaki,T
通讯作者：
Yonesaki,T