Wakem L P, Zahradka C L, Ebisuzaki K
Virology. 1984 Sep;137(2):338-46. doi: 10.1016/0042-6822(84)90226-5.
The requirement of DNA repair-recombination functions for T4 phage DNA replication has been known for some time but the underlying basis for this relationship has been unclear. This report is concerned with a new uv-sensitive gene [uvsU], whose function appears to bridge these two major activities of DNA. The [uvsU] mutant fails to complement [uvsX] mutants but uvsU maps in a region distinct from uvsX. Furthermore, the uvsU mutation specifically suppressed the DNA replication defect but not the uv sensitivity of the uvsX mutation. The previously discovered uvsW gene, whose mutations suppress the DNA replication defects of gene 59, 46, and 47 mutations, seems to have an analogous role. As a possible explanation for these observations, it is suggested that the uvsW and uvsU gene products (gps) couple the DNA repair-recombination and replication functions by controlling the entry of DNA intermediates from the replication pool into the DNA repair-recombination pathway. Furthermore the suppression data are interpreted to suggest that the gps uvsW, 59, 46, and 47 function together. Similarly the gps uvsU and uvsX may form a functional unit.
一段时间以来,人们已经知道T4噬菌体DNA复制需要DNA修复 - 重组功能,但这种关系的潜在基础尚不清楚。本报告关注一个新的对紫外线敏感的基因[uvsU],其功能似乎在DNA的这两个主要活动之间起到桥梁作用。[uvsU]突变体不能互补[uvsX]突变体,但uvsU定位于与uvsX不同的区域。此外,uvsU突变特异性地抑制了DNA复制缺陷,但没有抑制uvsX突变的紫外线敏感性。先前发现的uvsW基因,其突变抑制基因59、46和47突变的DNA复制缺陷,似乎具有类似的作用。作为对这些观察结果的一种可能解释,有人提出uvsW和uvsU基因产物(gp)通过控制DNA中间体从复制池进入DNA修复 - 重组途径,将DNA修复 - 重组和复制功能联系起来。此外,抑制数据被解释为表明uvsW、59、46和47的gp共同发挥作用。同样,uvsU和uvsX的gp可能形成一个功能单元。