Nissani M
Genetics. 1977 Aug;86(4):779-87. doi: 10.1093/genetics/86.4.779.
This paper draws attention to the formal parallelism that exists between chromosomal-loss mosaicism and mutagenically induced mosaicism in Drosophila and suggests that, although the underlying processes by which these two types of genetic mosaics are generated are very different, the more refined methodology employed in developmental analyses of genetically induced chromosomal-loss mosaics may be profitably extrapolated to mutagenesis studies. Results obtained from various studies of genetically induced mosaics and from a previous EMS mutation induction experiment at the yellow locus are utilized to illustrate this methodology and to estimate the total mutagenicity rates of EMS.-The following are some of the tentative conclusions that have been drawn in this report regarding an EMS concentration that produced 31% F(2) lethals in the standard X-linked recessive lethal test: (1) The frequency of cuticular mosaics is at least 5 times that of F(3) lethals. (2) At least 60% of all cuticular mosaics go undetected in the standard X -linked recessive lethal test since their mutant tissue does not extend into the germ line. (3) The frequency of EMS-induced cryptic mosaics is probably less than 10% the frequency of cuticular mosaics. (4) Some EMS-induced mutations are probably bona fide completes; if confirmed, this inference must be taken into consideration in estimating the total mutagenicity rates of this agent and in molecular interpretations of its mechanism of action. (5) The fact that the proportion of mutant tissue in EMS-induced mosaics is greater than 25% is consistent with the suggestion that the action of EMS is occasionally delayed until after the first cleavage division of the embryo. (6) Such an EMS concentration causes on the average more than 5 independent genetic alterations in the entire haploid genome of an X-bearing sperm.-This report clarifies the experimental evidence that must be generated, and the methodology that can be used to analyze this evidence, if it is of interest to render these and related conclusions regarding the effect of EMS on D. melanogaster more accurate, or if it is of interest to conduct a similar analysis for other mutagens that cause a significant degree of mosaicism.
本文关注了果蝇中染色体丢失嵌合体与诱变诱导嵌合体之间存在的形式上的平行关系,并表明,尽管产生这两种类型遗传嵌合体的潜在过程非常不同,但在遗传诱导的染色体丢失嵌合体的发育分析中采用的更精细方法可能有益地外推到诱变研究中。从各种遗传诱导嵌合体研究以及先前在黄色基因座进行的EMS突变诱导实验中获得的结果,被用于说明这种方法并估计EMS的总诱变率。以下是本报告中就标准X连锁隐性致死试验中产生31% F(2) 致死率的EMS浓度得出的一些初步结论:(1) 表皮嵌合体的频率至少是F(3) 致死率的5倍。(2) 在标准X连锁隐性致死试验中,所有表皮嵌合体中至少60% 未被检测到,因为它们的突变组织没有延伸到生殖系。(3) EMS诱导的隐性嵌合体的频率可能不到表皮嵌合体频率的10%。(4) 一些EMS诱导的突变可能是真正的完全突变;如果得到证实,在估计该诱变剂的总诱变率及其作用机制的分子解释中,必须考虑这一推断。(5) EMS诱导的嵌合体中突变组织的比例大于25% 这一事实,与EMS的作用偶尔会延迟到胚胎第一次卵裂分裂之后的观点一致。(6) 这样的EMS浓度平均会在携带X染色体的精子的整个单倍体基因组中引起超过5次独立的遗传改变。本报告阐明了,如果想要使这些以及关于EMS对黑腹果蝇影响的相关结论更准确,或者如果想要对导致显著程度嵌合体的其他诱变剂进行类似分析,必须生成的实验证据以及可用于分析该证据的方法。