The question of the total gene number in Drosophila melanogaster.
The question of the total gene number in Drosophila melanogaster.
复制标题
果蝇基因总数的问题。
作者：
George Lefevre;William Watkins
本文对近500个由G.勒费弗这些突变是在X染色体的四个不同区域诱导的：（1）1A 1 - 3E 8、（2）6D 1 - 8A 5、（3）9 E1 - 11 A7和（4）19 A1 - 20 F4，它们共同构成了整个染色体的三分之一以上。--分析表明，在不同的基因座发现的等位基因的数量不符合泊松分布，即使采取适当的程序，以适应截断性质的数据。然而，等位基因分布符合截尾负二项分布相当好，细胞学正常突变拟合比重排突变。这表明基因不是等变的，因为数据需要拟合泊松分布。使用负二项参数来估计在我们的实验中没有产生可检测的致死突变的基因的数量（n 0）给出了比使用泊松参数得到的更大的数字。不幸的是，我们不能估计非重要基因座的总数，基因座与不可检测的表型和基因座具有极低的变异性。无论如何，我们对生命基因总数的估计远远低于分析区域中的条带总数;然而，在几个短的时间间隔内，我们发现了比条带更多的生命基因;在其他时间间隔内，更少。我们的结论是，单带，单基因假说，在其字面意义上，是不正确的;此外，它很难支持，甚至近似。毫无疑问，果蝇基因总数的问题最终将通过分子分析来解决，而不是通过突变数据的统计分析或饱和研究。
A statistical analysis has been carried out on the distribution and allelism of nearly 500 sex-linked, X-ray-induced, cytologically normal and rearranged lethal mutations in Drosophila melanogaster that were obtained by G. Lefevre. The mutations were induced in four different regions of the X chromosome: (1) 1A1-3E8, (2) 6D1-8A5, (3) 9E1-11A7 and (4) 19A1-20F4, which together comprise more than one-third of the entire chromosome.--The analysis shows that the number of alleles found at different loci does not fit a Poisson distribution, even when the proper procedures are taken to accommodate the truncated nature of the data. However, the allele distribution fits a truncated negative binomial distribution quite well, with cytologically normal mutations fitting better than rearrangement mutations. This indicates that genes are not equimutable, as required for the data to fit a Poisson distribution.--Using the negative binomial parameters to estimate the number of genes that did not produce a detectable lethal mutation in our experiment (n0) gave a larger number than that derived from the use of the Poisson parameter. Unfortunately, we cannot estimate the total numbers of nonvital loci, loci with undetectable phenotypes and loci having extremely low mutabilities. In any event, our estimate of the total vital gene number was far short of the total number of bands in the analyzed regions; yet, in several short intervals, we have found more vital genes than bands; in other intervals, fewer. We conclude that the one-band, one-gene hypothesis, in its literal sense, is not true; furthermore, it is difficult to support, even approximately.--The question of the total gene number in Drosophila will, not doubt, eventually be solved by molecular analyses, not by statistical analysis of mutation data or saturation studies.