Meiotic Recombination in Drosophila

在此输入文本，它是您的应用程序的新摘要信息。此部分必须为no 超过30行的文本。 杂交直接影响减数分裂染色体的准确分离。几十年 的努力导致了一个详细的模型，概述了减数分裂重组的机制。 这几乎完全是基于对单一模式生物体所做的研究 发芽酵母酿酒酵母。我们最近测试了此模型的关键功能 后生果蝇黑腹果蝇。为了做到这一点，我们剔除了两个经典(长- 补丁)和短补丁失配修复，这是第一次在后生动物中这样做。 我们的结果提出了一种新的模型，该模型与 萌芽酵母模型。在目标1中，我们测试了我们模型的关键预测。为了做到这一点，我们 在没有错配修复的情况下检查全基因组减数分裂重组。我们会 对母体单倍体胚胎和母体单倍体胚胎进行排序 一个主染色体的二倍体，本质上是半四分体分析。我们也已经 最近的发现为理解交叉开辟了一条新的途径 位置受到控制。我们发现布卢姆综合征解旋酶(BLM)和一个复合体 我们称之为减数分裂-MCM(mei-MCM)复合体，两者都是正常交换所必需的 定位；在突变体中，交换是沿着染色体臂随机分布的 甚至发生在4号染色体上，通常没有减数分裂交叉。我们 假设BLM控制修复途径的选择；我们在AIM中验证了这一假设 3.我们发现MEI-MCM复合体是正常交换所必需的 调节，但这不需要ATPase活性(这一活动是必不可少的 跨界，只是不是为了分发它们)。在目标3中，我们继续阐明 交叉控制中的梅-MCM综合体，包括在 着丝粒和4号染色体上。这些实验的结果将带来新的曙光 关于减数分裂重组机制的研究，并为调控提供了新的见解 交叉放置。

Enter the text here that is the new abstract information for your application. This section must be no longer than 30 lines of text. Crossovers direct the accurate segregation of meiotic chromosomes. Several decades of effort has led to a detailed model outlining the mechanism of meiotic recombination. This is based almost entirely on research done with a single model organism, the budding yeast S. cerevisiae. We recently tested key features of this model in the metazoan Drosophila melanogaster. To do this, we knocked out both canonical (long- patch) and short-patch mismatch repair, the first time this has been done in a metazoan. Our results suggested a new model, one that has some fundamental differences from the budding yeast model. In Aim 1 we test key predictions of our model. To do this, we examine genome-wide meiotic recombination in the absence of mismatch repair. We will sequence maternally haploid embryos and also maternally haploid embryos that are disomic for one major chromosome, which is essentially half-tetrad analysis. We've also made recent discoveries that open up a new avenue to understanding how crossover position is controlled. We found that the Bloom syndrome helicase (BLM) and a complex we call the meiotic-MCM (mei-MCM) complex are both required for normal crossover positioning; in mutants, crossovers are distributed randomly along a chromosome arm and even occur on chromosome 4, which normally has no meiotic crossovers. We hypothesize that BLM controls choice of repair pathway; we test this hypothesis in Aim 3. We found that the mei-MCM complex is physically required for normal crossover regulation, but this does not require ATPase activity (this activity is essential for making crossovers, just not for distributing them). In Aim 3 we continue to elucidate functions of the mei-MCM complex in crossover control, including blocking crossover near the centromere and on chromosome 4. Results from these experiments will shed new light on meiotic recombination mechanisms and provide novel insights into regulation of crossover placement.