Ghisotti D, Chiaramonte R, Forti F, Zangrossi S, Sironi G, Dehò G
Dipartimento di Genetica e di Biologia dei Microrganismi, Università di Milano, Italy.
Mol Microbiol. 1992 Nov;6(22):3405-13. doi: 10.1111/j.1365-2958.1992.tb02208.x.
In the prophage P4, expression of the early genes is prevented by premature termination of transcription from the constitutive promoter PLE. In order to identify the region coding for the immunity determinant, we cloned several fragments of P4 DNA and tested their ability to confer immunity to P4 superinfection. A 357 bp long fragment (P4 8418-8774) is sufficient to confer immunity to an infecting P4 phage and to complement the immunity-defective P4 cl405 mutant, both in the presence and in the absence of the helper phage P2. The immunity region covers PLE and the cl locus. We were unable to obtain evidence of translation of the region, thus we suggest that P4 immunity is not elicited by a protein but by a transcript (or transcripts) encoded by the region downstream of the promoter PLE. The promoter PLE appears to be necessary for the expression of P4 immunity: fragments in which the PLE region is deleted did not complement P4 cl405 for lysogenization, although they still interfered with P4 growth. Two complementary sequences downstream of PLE (seqA and seqB) at the 5' and 3' ends of the immunity region play an essential role in the control of P4 immunity.
在原噬菌体P4中,早期基因的表达因组成型启动子PLE转录的提前终止而受到抑制。为了鉴定编码免疫决定簇的区域,我们克隆了P4 DNA的几个片段,并测试了它们赋予对P4超感染免疫的能力。一个357 bp长的片段(P4 8418 - 8774)足以赋予对感染性P4噬菌体的免疫能力,并在有和没有辅助噬菌体P2的情况下互补免疫缺陷型P4 cl405突变体。免疫区域覆盖PLE和cl基因座。我们无法获得该区域翻译的证据,因此我们认为P4免疫不是由一种蛋白质引发的,而是由启动子PLE下游区域编码的一种转录本(或多种转录本)引发的。启动子PLE似乎对P4免疫的表达是必需的:删除了PLE区域的片段不能互补P4 cl405进行溶原化,尽管它们仍然会干扰P4的生长。免疫区域5'和3'端PLE下游的两个互补序列(seqA和seqB)在P4免疫的控制中起重要作用。