PROCESS OF INFECTION WITH COLIPHAGE-T7 .5. SHUTOFF OF HOST RNA SYNTHESIS BY AN EARLY PHAGE FUNCTION

PROCESS OF INFECTION WITH COLIPHAGE-T7 .5. SHUTOFF OF HOST RNA SYNTHESIS BY AN EARLY PHAGE FUNCTION
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DOI:
10.1016/0042-6822(71)90129-2
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发表时间:
1971-01-01
期刊:
影响因子:
3.7
通讯作者:
SUMMERS, WC
SUMMERS, WC
中科院分区:
医学3区
文献类型:
--
作者:
BRUNOVSKIS, I;SUMMERS, WC

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用大肠杆菌噬菌体T7的基因1缺陷突变体感染大肠杆菌B导致宿主mRNA合成的抑制。从感染的细胞噬菌体和宿主DNA的脉冲标记的RNA的杂交表明,关闭的宿主mRNA的动力学是相同的感染与野生型噬菌体和琥珀或温度敏感的基因1突变体。在低感染复数下,氯霉素或嘌呤霉素阻止关闭,表明需要噬菌体编码的蛋白质。在较高的多重性,有一个氯霉素独立的,多重性依赖性抑制翻译。然而,在低多重性下,不阻止预制lacmRNA的翻译。由于在非允许条件下,除了失活的基因1产物外,基因1突变体仅编码两种或三种其他早期蛋白质,因此其中一种或多种似乎是负责关闭宿主mRNA合成的蛋白质的可能候选者。
Infection ofEscherichia coliB with gene 1 defective mutants of coliphage T7 results in inhibition of host mRNA synthesis. Hybridization of pulse-labeled RNA from infected cells to phage and host DNA shows that the kinetics of shutoff of host mRNA are identical in infections with wild-type phage and either amber or temperature-sensitive gene 1 mutants. At low multiplicities of infection, chloramphenicol or puromycin prevent the shut off, indicating a requirement for a phage-coded protein (s). At higher multiplicities, there is a chloramphenicol-independent, multiplicity-dependent inhibition of translation. However, at low multiplicity, translation of preformedlacmRNA is not prevented. Since, under nonpermissive conditions, gene 1 mutants code for only two or three other early proteins in addition to the inactive gene 1 product, one or more of these appear to be a likely candidate for the protein responsible for turning off host mRNA synthesis.