Skurray R A, Willetts N, Reeves P
Mol Gen Genet. 1976 Jul 23;146(2):161-5. doi: 10.1007/BF00268084.
Hfr, F+, and F-prime cells are, unlike F- cells, insensitive to an excess of Hfr donor cells, indicating that there is an F factor mediated immunity to lethal zygosis (I1z). Results with Flac episomes carrying traJ, traS or various polar mutations in the tra region indicate that this immunity is independent of surface exclusion, of traJ control, and of all known genes within the tra operon. However, analysis of a series of strains with deletions in the F factor, extending from the right into the tra region, suggests that a gene for immunity to lethal zygosis is located within the tra region. We therefore conclude that I1z is genetically complex, and present a hypothesis to account for these results.
与F-细胞不同,高频重组(Hfr)细胞、F+细胞和F' 细胞对过量的Hfr供体细胞不敏感,这表明存在一种由F因子介导的对致死合子形成(I1z)的免疫性。携带traJ、traS或tra区域各种极性突变的Flac附加体的实验结果表明,这种免疫性独立于表面排斥、traJ调控以及tra操纵子内所有已知基因。然而,对一系列F因子发生从右侧延伸至tra区域缺失的菌株进行分析表明,致死合子形成免疫基因位于tra区域内。因此,我们得出结论,I1z在遗传上是复杂的,并提出一个假说来解释这些结果。