Department of Biology, McGill University, Montreal, Canada H3A 1B1.
Genetics. 1983 Sep;105(1):19-33. doi: 10.1093/genetics/105.1.19.
The nuclease halo mutant, nuh-4, of Neurospora crassa was identified conclusively as an allele of uvs-3, a gene involved in error-prone DNA repair. Like uvs-3, nuh-4 showed spontaneous mutator effects, and any previous contradictory findings were found to be due to newly arisen mutants. In normal strains the two alleles are noncomplementing and indistinguishable for sensitivity to UV and methyl methanesulfonate (MMS). Like uvs-3, nuh-4 lacked secretion of the extracellular enzyme, DNase A, a Ca(++)-dependent strand-nonspecific endonuclease which was found to be phosphate repressible. However, nuh-4 differed from uvs-3 in showing much higher conidial viability and lower sensitivity to ionizing radiation and mitomycin C.--Epistatic relationships of the two uvs-3 alleles with seven other MMS-sensitive mutants were determined and compared with those of the highly X-ray-sensitive mutant, uvs-6. Three epistatic groups were found, based on survival of double mutant strains relative to that of their component single mutant strains after treatment with MMS. Both, uvs-3 and nuh-4, were epistatic to mus-9 which also is a mutator. None of the three produced viable double mutants in crosses to uvs-6. On the other hand, uvs-6, but not the uvs-3 alleles, was found to be epistatic to mus-7 and mus-10. The excision-defective uvs-2 and mus-8 both showed synergism with the uvs-3 alleles and with uvs-6, forming a third, separate epistatic group.
粗糙脉孢菌的核酸酶晕突变体 nuh-4 被明确鉴定为 uvs-3 的等位基因,uvs-3 基因参与易错 DNA 修复。与 uvs-3 一样,nuh-4 表现出自发的突变体效应,任何先前的矛盾发现都归因于新出现的突变体。在正常菌株中,这两个等位基因是非互补的,并且对 UV 和甲磺酸甲酯(MMS)的敏感性无法区分。与 uvs-3 一样,nuh-4 缺乏细胞外酶 DNase A 的分泌,DNase A 是一种依赖 Ca(++)的非特异性链内切酶,发现其受磷酸盐抑制。然而,nuh-4 与 uvs-3 的不同之处在于具有更高的分生孢子活力和对电离辐射和丝裂霉素 C 的敏感性较低。--这两个 uvs-3 等位基因与其他七个 MMS 敏感突变体的上位性关系被确定,并与高度 X 射线敏感突变体 uvs-6 进行了比较。基于 MMS 处理后双突变株系相对于其组成单突变株系的存活率,发现了三个上位性组。uvs-3 和 nuh-4 都与 mut-9 上位性,mut-9 也是一个诱变剂。在与 uvs-6 的杂交中,这三个都没有产生有活力的双突变体。另一方面,发现 uvs-6 而不是 uvs-3 等位基因与 mut-7 和 mut-10 上位性。切除缺陷 uvs-2 和 mut-8 都与 uvs-3 等位基因和 uvs-6 表现出协同作用,形成第三个独立的上位性组。