Inoue H, Ong T M, de Serres F J
Mutat Res. 1981 Jan;80(1):27-41. doi: 10.1016/0027-5107(81)90175-5.
The genetic effects of MNNG, 4NQO and ICR-170 have been compared on 5 different UV-sensitive strains and a standard wild-type strain of Neurospora crassa with regard to inactivation and the induction of forward-mutations at the ad-3A and ad-3B loci. Whereas all UV-sensitive strains (upr-1, uvs-2, uvs-3, uvs-5 and uvs-6) are more sensitive to inactivation by MNNG and ICR-170 than wild-type, only uvs-5 shows survival comparable to wild-type after 4NQO treatment, all other strains are more sensitive to 4NQO. In contrast to the effects on inactivation, a wide variety of effects were found for the induction of ad-3A and ad-3B mutations: higher forward-mutation frequencies than were found in wild-type were obtained after treatment with MNNG or 4NQO for upr-1 and uvs-2, no significant increase over the spontaneous mutation frequency was found with uvs-3 after MNNG, 4NQO or ICR-170 treatment; mutation frequencies comparable to that found in wild-type were obtained with uvs-6 after MNNG, 4NQO or ICR-170 treatment and with upr-1 after ICR-170 treatment. Lower forward-mutation frequencies than were found in wild-type were obtained with uvs-2 after ICR-170 treatment and with uvs-5 after MNNG, 4NQO or ICR-170 treatment. These data clearly show that the process of forward-mutation at the ad-3A and ad-3B loci is under genetic control by mutations at other loci (e.g. upr-1, uvs-2, uvs-3, uvs-5 and uvs-6) and that the effect is markedly mutagen-dependent.
已比较了甲基硝基亚硝基胍(MNNG)、4-硝基喹啉-1-氧化物(4NQO)和ICR-170对粗糙脉孢菌5种不同的紫外线敏感菌株及一种标准野生型菌株在ad-3A和ad-3B位点的失活作用及正向突变诱导方面的遗传效应。所有紫外线敏感菌株(upr-1、uvs-2、uvs-3、uvs-5和uvs-6)对MNNG和ICR-170失活作用的敏感性均高于野生型,而只有uvs-5在4NQO处理后显示出与野生型相当的存活率,所有其他菌株对4NQO更敏感。与对失活的影响相反,在ad-3A和ad-3B突变诱导方面发现了多种效应:用MNNG或4NQO处理后,upr-1和uvs-2的正向突变频率高于野生型;uvs-3在MNNG、4NQO或ICR-170处理后,其突变频率与自发突变频率相比无显著增加;uvs-6在MNNG、4NQO或ICR-170处理后以及upr-1在ICR-170处理后的突变频率与野生型相当。uvs-2在ICR-170处理后以及uvs-5在MNNG、4NQO或ICR-170处理后的正向突变频率低于野生型。这些数据清楚地表明,ad-3A和ad-3B位点的正向突变过程受其他位点(如upr-1、uvs-2、uvs-3、uvs-5和uvs-6)突变的遗传控制,且该效应明显依赖于诱变剂。