Rex-dependent exclusion of lambdoid phages. II. Determinants of sensitivity to exclusion.

Rex-dependent exclusion of lambdoid phages. II. Determinants of sensitivity to exclusion.
复制标题

雷克斯依赖性的羔羊噬菌体排除。

DOI:
10.1016/0042-6822(80)90077-x
复制
发表时间:
1980
期刊:
影响因子:
3.7
通讯作者:
I. Herskowitz
I. Herskowitz
中科院分区:
医学3区
文献类型:
--
作者:
P. Toothman;I. Herskowitz

文献摘要

被引文献

相似文献

对Rex依赖排斥敏感的Lambdoid噬菌体和突变体已经被鉴定和鉴定。至少需要两个λ基因RedRen才能完全保护λ免受REX依赖的排斥。突变是隐性的,位于基因PandQ之间,可能定义一个新基因。λ-P22和λ-θ80杂交种用P22或θ80DNA替换λ基因0和P以及P-Q区的一部分,对REX依赖排斥反应敏感,携带缺失(NIN5)的噬菌体也是如此。互补试验表明,这些噬菌体均为表型为REN的−。对Rex敏感的第二类突变体是红色−,即在噬菌体通用重组系统中存在缺陷。因此,似乎有几个噬菌体λ、T5、T7和T4产生的功能(Renandred、LR、Rb1、Andrii的产物)允许噬菌体在Rex存在的情况下生长。由于REX-REN功能是一种已知的λ核酸酶,它保护λ免受REX依赖的排斥,我们认为RED和REN可能通过阻止对REX敏感的底物的形成或修复已被REX作用的底物而起作用。在λ和P22复制基因0(18)和P(12)中发现了抑制突变,它们允许红色−或REN−噬菌体在Rex存在的情况下生长。这些突变体中的一些已经获得了它们的生长受到Rex刺激的特性,在某些情况下,它们依赖于Rex。这些观察结果表明,Rex可以取代或补偿限制0和P的活性。
Lambdoid phages and mutants sensitive to Rex-dependent exclusion have been identified and characterized. At least two λ genes,redandren, are required for full protection of λ from Rex-dependent exclusion.Renmutations, which are recessive and are located between genesPandQ, may define a new gene. λ-P22 and λ-θ80 hybrids with P22 or θ80 DNA substituted for λ genes 0 andPand part of theP-Qregion are sensitive to Rex-dependent exclusion, as are phages carrying a deletion (nin5) betweenPandQ. Complementation tests show that these phages are phenotypically Ren−. The second class of mutants sensitive to Rex are Red−, that is, defective in the phage general recombination system. Thus it appears that several phages, λ, T5, T7, and T4, produce functions (products ofrenandred, lr, rbl, andrII) which allow phage growth in the presence of Rex. Because λ Red function, a known DNA nuclease, protects λ from Rex-dependent exclusion, we propose that Red and Ren may act by preventing formation of a DNA substrate which is sensitive to Rex or by repairing a DNA substrate which has been acted on by Rex. Suppressor mutations have been identified in λ and P22 replication genes,0(18)andP(12), which allow Red−or Ren−phage to grow in the presence of Rex. Some of these mutants have acquired the property that their growth is stimulated by Rex and, in some cases, is dependent on Rex. These observations suggest that Rex can replace or compensate for limiting 0 and P activity.