Thurm P, Garro A J
J Virol. 1975 Jul;16(1):184-91. doi: 10.1128/JVI.16.1.184-191.1975.
Bacillus subtilis mutants with lesions in PBSX prophage genes have been isolated. One of these appears to be a regulatory mutant and is defective for mitomycin C-induced derepression of PBSX; the others are defective for phage capsid formation. All of the PBSX structural proteins are synthesized during induction of the capsid defective mutants; however, several of these proteins exhibit abnormal serological reactivity with anti-PBSX antiserum. The two head proteins X4 and X7 are not immunoprecipitable in a mutant which fails to assemble phage head structures. In the tail mutant, proteins X5 and X6 are not immunoprecipitable, tails are not assembled, and a possible tail protein precursor remains uncleaved. The noninducible mutant does not synthesize any PBSX structural proteins after exposure to mitomycin C. The mutation is specific for PBSX since ø105 and SPO2 lysogens of the mutant are inducible. All of the known PBSX-specific mutations were shown to be clustered between argC and metC on the host chromosome. In addition, the metC marker was shown to be present in multiple copies in cells induced for PBSX replication. This suggests that the derepressed prophage replicates while still integrated and that replication extends into the adjacent regions of the host chromosome.
已分离出在PBSX原噬菌体基因中存在损伤的枯草芽孢杆菌突变体。其中一个似乎是调节突变体,对丝裂霉素C诱导的PBSX去阻遏有缺陷;其他的则在噬菌体衣壳形成方面有缺陷。在衣壳缺陷突变体诱导过程中会合成所有PBSX结构蛋白;然而,其中几种蛋白与抗PBSX抗血清表现出异常的血清学反应性。在一个无法组装噬菌体头部结构的突变体中,两种头部蛋白X4和X7不可被免疫沉淀。在尾部突变体中,蛋白X5和X6不可被免疫沉淀,尾部无法组装,并且一种可能的尾部蛋白前体仍未被切割。不可诱导的突变体在暴露于丝裂霉素C后不合成任何PBSX结构蛋白。该突变对PBSX具有特异性,因为该突变体的ø105和SPO2溶原菌是可诱导的。所有已知的PBSX特异性突变都显示聚集在宿主染色体上的argC和metC之间。此外,在诱导PBSX复制的细胞中,metC标记显示存在多个拷贝。这表明去阻遏的原噬菌体在仍整合时进行复制,并且复制延伸到宿主染色体的相邻区域。