rIIa和rIIb突变对T4D连接酶突变的抑制作用。
Suppression of T4D ligase mutations by rIIa and rIIb mutations.
作者信息
Berger H, Kozinski A W
出版信息
Proc Natl Acad Sci U S A. 1969 Nov;64(3):897-904. doi: 10.1073/pnas.64.3.897.
Abstract
The introduction of rII mutations into polynucleotide ligase amber mutants (gene 30) of T4D bacteriophage results in the restoration of phage growth in the nonpermissive host E. coli B. When cells are mixedly infected with rII(+) -ligase(-) and rII-ligase(-) phage, growth is reduced, indicating that the rII mutations are recessive to the rII(+) alleles. Infection with the rII-ligase(-) double mutants results in nearly complete restoration of phage DNA synthesis and prevents the extensive degradation of parental phage DNA observed after infection with ligase(-) single mutants. Similar results are observed when cells are infected with ligase(-) mutants and chloramphenicol is added five minutes post infection.
摘要
将rII突变引入T4D噬菌体的多核苷酸连接酶琥珀突变体（基因30）中，可使噬菌体在非允许宿主大肠杆菌B中恢复生长。当细胞被rII(+) -连接酶(-)和rII-连接酶(-)噬菌体混合感染时，生长会受到抑制，这表明rII突变相对于rII(+)等位基因是隐性的。用rII-连接酶(-)双突变体感染可使噬菌体DNA合成几乎完全恢复，并防止在感染连接酶(-)单突变体后观察到的亲本噬菌体DNA的大量降解。当细胞被连接酶(-)突变体感染并在感染后五分钟添加氯霉素时，也会观察到类似的结果。
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