Brockman H E, de Serres F J
Department of Biological Sciences, Illinois State University, Normal 61761.
Mutat Res. 1991 Jan;246(1):193-204. doi: 10.1016/0027-5107(91)90122-5.
Procarbazine (Natulan) was tested for its mutagenic potency and specificity in the ad-3 forward-mutation test in heterokaryon 12 (H-12) of Neurospora crassa. In these experiments, procarbazine was a weak mutagen when present in growing cultures but nonmutagenic when conidial suspensions (nongrowing conidia) were treated. A total of 208 ad-3 mutants recovered after exposure of growing cultures of H-12 to 1 mg of procarbazine/ml, and 2 ad-3 mutants of spontaneous origin, were characterized genetically. These tests distinguish among gene/point mutations (ad-3R) at the ad-3A or ad-3B locus, multilocus deletion mutations ([ad-3]IR) covering one or more loci in the ad-3 and immediately adjacent regions, and 3 different classes of multiple-locus mutations: gene/point ad-3 mutations with a recessive lethal mutation elsewhere in the genome (ad-3R + RL), gene/point mutations with a closely linked recessive lethal mutation (ad-3R + RLCL), and multilocus deletion mutations with a closely linked recessive lethal mutation ([ad-3]IR + RLCL). All of the procarbazine-induced ad-3 mutants resulted from gene/point mutations; 92.2% (200/217) resulted from gene/point mutations at the ad-3A or ad-3B locus, and 3.7% (8/217) resulted from gene/point mutations with a recessive lethal mutation elsewhere in the genome. Identical percentages (15.4% [20/130] and 15.4% [12/78]) of the sigma ad-3BR and sigma ad-3AR mutants were leaky, and a high percentage (71.5% [93/130]) of the sigma ad-3BR mutants had nonpolarized complementation patterns. These results indicate that procarbazine-induced ad-3 mutants of Neurospora crassa are composed solely of gene/point mutations (ad-3R) that resulted, predominantly or exclusively, from base-pair substitutions. The Neurospora specific-locus data on procarbazine-induced ad-3 mutants are compared with data from similar experiments with the mouse using the morphological specific-locus assay; marked similarities were found between the mutagenic effects of procarbazine in the 2 specific-locus assays.
在粗糙脉孢菌异核体12（H - 12）的ad - 3正向突变试验中，对丙卡巴肼（纳治兰）的诱变效力和特异性进行了测试。在这些实验中，当丙卡巴肼存在于生长培养物中时，它是一种弱诱变剂，但当处理分生孢子悬液（非生长的分生孢子）时则无诱变作用。将H - 12的生长培养物暴露于1mg/ml的丙卡巴肼后，共获得208个ad - 3突变体，以及2个自发产生的ad - 3突变体，并对其进行了遗传学特征分析。这些测试可区分ad - 3A或ad - 3B位点的基因/点突变（ad - 3R）、覆盖ad - 3及其紧邻区域一个或多个位点的多位点缺失突变（[ad - 3]IR），以及3种不同类型的多位点突变：基因组其他位置带有隐性致死突变的基因/点ad - 3突变（ad - 3R + RL）、带有紧密连锁隐性致死突变的基因/点突变（ad - 3R + RLCL），以及带有紧密连锁隐性致死突变的多位点缺失突变（[ad - 3]IR + RLCL）。所有丙卡巴肼诱导的ad - 3突变体均由基因/点突变产生；92.2%（200/217）是由ad - 3A或ad - 3B位点的基因/点突变引起的，3.7%（8/217）是由基因组其他位置带有隐性致死突变的基因/点突变引起的。σad - 3BR和σad - 3AR突变体中相同比例（15.4% [20/130]和15.4% [12/78]）为渗漏型，且σad - 3BR突变体中有高比例（71.5% [93/130]）具有非极化互补模式。这些结果表明，丙卡巴肼诱导的粗糙脉孢菌ad - 3突变体仅由基因/点突变（ad - 3R）组成，这些突变主要或完全由碱基对替换导致。将丙卡巴肼诱导的粗糙脉孢菌ad - 3突变体的脉孢菌特异性位点数据与使用形态学特异性位点测定法对小鼠进行的类似实验数据进行了比较；在这两种特异性位点测定法中，发现丙卡巴肼的诱变效应存在显著相似性。
