Zoology Department, Michigan State University, East Lansing, Michigan 48824.
Genetics. 1984 Mar;106(3):403-22. doi: 10.1093/genetics/106.3.403.
In Drosophila melanogaster males, deficiency for X heterochromatin causes high X-Y nondisjunction and skewed sex chromosome segregation ratios (meiotic drive). Y and XY classes are recovered poorly because of sperm dysfunction. In this study it was found that X heterochromatic deficiencies disrupt recovery not only of the Y chromosome but also of the X and autosomes, that both heterochromatic and euchromatic regions of chromosomes are affected and that the "sensitivity" of a chromosome to meiotic drive is a function of its length. Two models to explain these results are considered. One is a competitive model that proposes that all chromosomes must compete for a scarce chromosome-binding material in Xh(-) males. The failure to observe competitive interactions among chromosome recovery probabilities rules out this model. The second is a pairing model which holds that normal spermiogenesis requires X-Y pairing at special heterochromatic pairing sites. Unsaturated pairing sites become gametic lethals. This model fails to account for autosomal sensitivity to meiotic drive. It is also contradicted by evidence that saturation of Y-pairing sites fails to suppress meiotic drive in Xh(- ) males and that extra X-pairing sites in an otherwise normal male do not induce drive. It is argued that meiotic drive results from separation of X euchromatin from X heterochromatin.
在黑腹果蝇雄体中,X 异染色质的缺失会导致高 X-Y 不分离和性染色体分离比例偏斜(减数分裂驱动)。由于精子功能障碍,Y 和 XY 类精子回收不良。本研究发现,X 异染色质缺失不仅破坏了 Y 染色体的恢复,还破坏了 X 和常染色体的恢复,染色体的异染色质和常染色质区域都受到影响,并且染色体对减数分裂驱动的“敏感性”是其长度的函数。考虑了两种解释这些结果的模型。一种是竞争模型,该模型提出所有染色体在 Xh(-) 雄性中必须竞争稀缺的染色体结合材料。没有观察到染色体恢复概率之间的竞争相互作用排除了该模型。另一种是配对模型,该模型认为正常精子发生需要 X-Y 在特殊异染色质配对位点配对。不饱和配对位点成为配子致死。该模型不能解释常染色体对减数分裂驱动的敏感性。它也与以下证据相矛盾,即 Y-配对位点的饱和并不能抑制 Xh(-) 雄性中的减数分裂驱动,而在正常雄性中额外的 X-配对位点不会诱导驱动。有人认为,减数分裂驱动是由 X 常染色质与 X 异染色质的分离引起的。