MOLECULAR & EVOLUTIONARY GENETICS OF SEGREGATION DISTORT

黑腹果蝇的分离偏差(SD) 研究最深入的减数分裂驱动系统在染色体和 人口水平。我们现在准备好研究分子基础。 Sd.分子克隆也将带来更好的理解 这个系统的种群遗传学。的目标 分离扭曲是响应者(RSP)基因：等位基因在 这些基因座大致分为敏感或不敏感两类。我们 我发现100-1000个重复序列的串联阵列 到目前为止，已经检查了八条敏感染色体。的数组 所有被检查的8条不敏感的染色体中都没有重复。 已经对重复序列的七个拷贝进行了测序，这些拷贝代表了 一类新的卫星DNA及其在生物信息学中的作用 染色质凝聚和分离。一个反常的过程 凝结是生精失败的一个很可能的原因， 导致偏析扭曲。 我们建议从三个方面对RSP进行研究。I)进一步的分子 描述可吸入颗粒物基因座的极限。我们计划 使用不同结构的染色体，如缺失， 无移位复制以及自然发生的 变种，以实现这一目标。该序列充分以及 将确定敏感度所需的因素。我们的数据表明 序列不是别人，正是大量重复序列 我们将进一步检验这一假设 灵敏度是串联的大小的直接结果 数组。将对更多数量的重复进行排序 用于分子进化研究。二)进化和人口 将对SD的遗传学方面进行研究。我们将描述 近缘物种中RSP的结构。天然中的RSP等位基因 将对人口进行调查。四个实验人群将 被设置和监控。这些人口将代表 敏感染色体和不敏感染色体之间的竞争 在存在和不存在SD染色体的情况下。一颗卫星 放大假说，提出用来解释困惑 对SD的观察，将进行测试。三)分子机制 我们将探讨潜在的扭曲现象。我们将调查是否 RSP等位基因在扭曲和非扭曲条件下转录 条件。我们已经制定了一项长期计划来研究 与RSP卫星DNA相关的染色质结构。 在细胞系和细胞中与这种DNA结合的蛋白质的分析 计划了不同的组织。

Segregation Distorter (SD) of Drosophila melanogasteris one of the best studied meiotic drive systems at the chromosomal and population level. We are now ready to study the molecular basis of SD. Molecular cloning will also lead to a better understanding of the population genetics of this system. The target for segregation distortion is the Responder (Rsp) locus: the alleles at the locus are broadly classified as sensitive or insensitive. We have found that a tandem array of 100-1,000 repeats are in all eight sensitive chromosomes so far examined. The array of repeats are absent in all eight insensitive chromosomes examined. Seven copies of the repeats have been sequenced which represent a novel class of satellite DNA and its hypothetical roles in chromatin condensation and segregation. An aberrant process of condensation is a very likely cause of spermiogenic failure, resulting in segregation distortion. We propose to study three aspects of Rsp. I) Further molecular characterization to delineate the limit of the Rsp locus. We plan to use chromosomes of various construct, such as deletions, translocations free duplications as well as naturally-occurring variants, to achieve this goal. The sequences sufficient as well as necessary for sensitivity will be identified. Our data suggest such sequences are none other than the large array of repeats themselves and we will further test this hypothesis that sensitivity is a direct consequence of the size of the tandem array. Sequencing a larger number of repeats will be carried out for molecular evolution studies. II) Evolutionary and population genetic aspects of SD will be studied. We will characterize the structure of Rsp in closely related species. Rsp alleles in natural populations will be surveyed. Four experimental populations will be set up and monitored. These populations will represent competition between sensitive and insensitive chromosomes both in the presence and absence of SD chromosomes. A satellite amplification hypothesis, proposed to explain perplexing observations on SD, will be tested. III) Molecular mechanisms underlying distortion will be explored. We will investigate if the Rsp alleles are transcribed under distorting and nondistorting conditions. We have developed a long term plan to study the chromatin structure associated with the Rsp satellite DNA. Assays for proteins that bind to such DNA in cell lines and in different tissues are planned.