Mosig G
Genetics. 1985 Jun;110(2):159-71. doi: 10.1093/genetics/110.2.159.
Gene 32 of phage T4 has been shown previously to be involved in recombinational repair of UV damages but, based on a mutant study, was thought not to be required for excision repair. However, a comparison of UV-inactivation curves of several gene 32 mutants grown under conditions permissive for progeny production in wild-type or polA- hosts demonstrates that gene 32 participates in both kinds of repair. Different gene 32 mutations differentially inactivate these repair functions. Under conditions permissive for DNA replication and progeny production, all gene 32 mutants investigated here are partially defective in recombinational repair, whereas only two of them, P7 and P401, are also defective in excision repair. P401 is the only mutant whose final slope of the inactivation curve is significantly steeper than that of wild-type T4. These results are discussed in terms of interactions of gp32, a single-stranded DNA-binding protein, with DNA and with other proteins.
噬菌体T4的基因32先前已被证明参与紫外线损伤的重组修复,但基于一项突变体研究,曾被认为不是切除修复所必需的。然而,对在允许野生型或polA-宿主中产生子代的条件下生长的几个基因32突变体的紫外线失活曲线进行比较表明,基因32参与这两种修复。不同的基因32突变以不同方式使这些修复功能失活。在允许DNA复制和产生子代的条件下,这里研究的所有基因32突变体在重组修复方面都有部分缺陷,而其中只有两个,即P7和P401,在切除修复方面也有缺陷。P401是唯一其失活曲线最终斜率明显比野生型T4更陡的突变体。本文根据单链DNA结合蛋白gp32与DNA及其他蛋白质的相互作用对这些结果进行了讨论。