Cupido M, Grimbergen J, De Groot B
Mutat Res. 1980 Apr;70(2):131-8. doi: 10.1016/0027-5107(80)90152-9.
The location of the non-essential T4 mutant uvs79, with defective replication repair, is described. After crosses with double mutants dispersed over the early region of T4, a linkage was observed with the double mutant am41 : am42. For more accurate location, crosses were made with single mutants. Uvs79 proved to be located between mutants amC23 and amN81 in gene 41, as shown by 3-point crosses. No genetic complementation with respect to multiplicity reactivation was found between amN81 and uvs79 after co-infection of an su- host. Apparently, mutant amN81 is disturbed as to replication repair and, owing to its lack of DNA synthesis, also in replication-dependent recombination repair. Consequently, the product of gene 41 has a function additional to its RNA-primer induction during replication of undamaged DNA. Presumably, the product of gene 41 induces RNA primers opposite DNA regions containing lesions. This capability is believed to be specifically affected by the uvs79 mutation.
描述了具有缺陷复制修复功能的非必需T4突变体uvs79的定位。在与分散于T4早期区域的双突变体杂交后,观察到它与双突变体am41:am42存在连锁关系。为了更精确地定位,又与单突变体进行了杂交。三点杂交结果表明,uvs79位于基因41中的突变体amC23和amN81之间。在对一个su-宿主进行共感染后,未发现amN81和uvs79在多重复活方面存在遗传互补。显然,突变体amN81在复制修复方面受到干扰,并且由于其缺乏DNA合成,在依赖复制的重组修复中也受到影响。因此,基因41的产物在未受损DNA复制过程中除了诱导RNA引物外还有其他功能。据推测,基因41的产物在含有损伤的DNA区域对面诱导RNA引物。据信uvs79突变会特异性影响这种能力。