Evidence for sperm dysfunction as the mechanism of segregation distortion in Drosophila melanogaster.
Evidence for sperm dysfunction as the mechanism of segregation distortion in Drosophila melanogaster.
复制标题
精子功能障碍作为果蝇分离扭曲机制的证据。
DOI：
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发表时间：
1967
影响因子：
11.1
通讯作者：
J. Crow
中科院分区：
文献类型：
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作者：
D. Hartl;Y. Hiraizumi;J. Crow
分离扭曲(SD)第二染色体杂合子的雄性黑腹果蝇会产生大量的SD后代，在一些种群中SD后代的比例经常超过0.99。Sandler、Hiraizumi和Sandler的研究表明，SD现象是早合子的；最近的数据表明，SD现象在减数分裂1.2或接近减数分裂1.2的时候是温度敏感的，显然在那个时候发生了一些关键事件。SD作用机制的早期模型包括SD同源物的断裂和反向姐妹染色单体的形成。当在SD男性中发现X射线诱导的减数分裂交叉的频率高于可比对照时，这种断裂假说得到了一些支持。3然而，由于未能观察到黑化病中的这种细胞学异常，该模型受挫。另一种模型，孔雀和埃里克森的功能极假说，4首先提出正常雄性果蝇的初级精母细胞是极化的，其中一个后期I二分体形成两个正常功能精子，另一个二分体形成两个形态正常但没有功能的精子；第二，SD同源物优先指向非功能极。我们随后的讨论只涉及这一假设的后半部分，而根本不涉及精母细胞是否实际上是正常极化的。皮科克和埃里克森通过将储存在雌性体内的精子数量与由SD或非SD雄性受精的可比雌性获得的后代数量进行比较，提出了这一假说的论点。在SD和对照组中，似乎只有一半的储存精子能够受精。因此有两个普遍的假设：(1)接受非SD染色体的精子以某种方式变得不能遵循正常的过程最终导致受精，(2)接受非SD染色体的精子通常注定是无功能的；这里的主要事件是中期I的优先染色体取向。我们称之为功能障碍精子和功能极假设。功能障碍假说包括破裂作为一种可能性，但意在包括任何干扰正常精子发育或功能的机制。这两个假设不一定是排他性的：例如，可能只有一半的精子具有正常的功能，但SD造成了其中一半的功能障碍。在本文中，我们报告了在精子数量似乎是后代生产的限制因素的条件下，SD雄性产生的后代数量与扭曲程度之间的负相关关系。这一结果支持功能障碍假说。材料-来自大自然的原始SD染色体带有三个可分离的遗传元件的倒位连锁复合体：SD本身和位于第二染色体着丝粒附近的“激活子”(Ac(SD))，以及“稳定器”(ST(SD))。
Drosophila melanogaster males heterozygous for the segregation distorter (SD) second chromosome produce a gross excess of SD-bearing progeny, the percentage of SD progeny in some stocks regularly exceeding 0.99. Sandler, Hiraizumi, and Sandler' have shown the SD phenomenon to be prezygotic; more recent data have shown it to be temperature-sensitive in or near meiosis 1.2 Evidently some critical event occurs at about that time. An early model for the mechanism of SD action involves a fracture of the SD homologue and formation of a reversed sister-chromatid reunion.' Such a breakage hypothesis received some support when a higher frequency of X-ray-induced meiotic crossing over was found in SD males than in comparable controls.3 The model was frustrated, however, by the failure to observe such cytological abnormalities in melosis. An alternative model, the functional pole hypothesis of Peacock and Erickson,4 proposes first that the primary spermatocyte of normal Drosophila males is polarized, with one of the Anaphase I dyads forming two normal functional sperms, the other dyad forming two morphologically normal but nonfunctional sperms; and secondly that the SD homologue is preferentially directed to the nonfunctional pole. Our subsequent discussion concerns only this latter part of the hypothesis, and not at all whether the spermatocyte is, in fact, normally polarized. Peacock and Erickson have developed an argument for the hypothesis by comparing the number of sperms stored in females with the number of progeny obtained from comparable females inseminated by SD or non-SD males. In both SD and controls only one half of the stored sperms appeared to be capable of fertilization. There are thus two general hypotheses: (1) the sperms receiving the non-SD chromosome are somehow rendered unable to follow the normal course leading ultimately to fertilization, and (2) the sperms receiving the non-SD chromosome are normally destined to be nonfunctional; the primary event here is a preferential chromosome orientation at Metaphase I. We shall call these the dysfunctional sperm and the functional pole hypotheses. The dysfunction hypothesis includes a break as one possibility, but is intended to include any mechanism that interferes with normal sperm development or function. The two hypotheses are not necessarily exclusive: It could be, for example, that only one half of the sperms are normally functional but that SD makes half of these dysfunctional. In this paper we report a negative correlation between the degree of distortion and the number of offspring produced by an SD male under conditions where sperm number appears to be the limiting factor in progeny production. This result argues for the dysfunction hypothesis. Materials.-The original SD chromosomes from nature carry an inversion-linked complex of three separable genetic elements: SD itself and an "activator" (Ac(SD)) both located near the centromere of chromosome II, and a "stabilizer" (St(SD))