Polarity and meiotic exit in the early C. elegans embryo

早期线虫胚胎的极性和减数分裂退出

• 批准号: 6847682
• 负责人: REBECCA LYNN LYCZAK
• 金额: $ 17.19万
• 依托单位: URSINUS COLLEGE
• 依托单位国家: 美国
• 财政年份: 2005
• 资助国家: 美国
• 起止时间: 2005-05-01 至 2009-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6847682
• 关键词: Caenorhabditis elegans; RNA interference; cell cycle; cell cycle proteins; cellular polarity; developmental genetics; embryogenesis; embryogenic cleavage; enzyme activity; fertilization; gene mutation; helminth genetics; immunofluorescence technique; meiosis; mitogen activated protein kinase; molecular cloning; protein localization; protein protein interaction; protein structure function; sperm

DESCRIPTION (provided by applicant): Polarization of the anterior-posterior (A-P) body axis in the nematode Caenorhabditis elegans occurs shortly after fertilization and before onset of the first round of mitosis. This polarization event occurs in close succession following the completion of meiosis by the oocyte chromosomes. Interestingly, both meiotic completion and axis polarization are triggered by cues from the sperm, although very few sperm-supplied factors have been identified. Recent studies have suggested that meiotic exit defects often correlate with defects in axis establishment, suggesting that these two processes may be developmentally linked. Despite this, little is known about how these events are temporally regulated in the cell or possible interrationships between the two. To investigate this problem, the scu-1 (sperm cue abnormal) gene will be studied in C. elegans. Mutations in scu-1 result in both a meiotic exit defect and a failure to polarize the A-P axis. In addition, the scu-1 gene product is contributed both maternally and paternally which may lead to a better understanding of paternally supplied proteins. To uncover the mechanisms by which scu-1 regulates meioitic exit and axis polarization, research will focus on three specific aims. 1) The role of scu-1 during meiotic exit will be examined by testing the role for scu-1 in MAPK and MPF deactivation after meiosis, and by dissecting the maternal and paternal contributions of SCU-1 during meiosis. 2) The molecular identity of the scu-1 gene and the subcellular localization of the protein will be determined through molecular cloning and antibody production and staining 3) SCU-1 interacting proteins will be identified though genetic suppressor screens and a genome-wide RNA interference screen for enhancers. These studies should provide insights into the mechanisms controlling the coordination of the cell cycle and polarity in the early embryo.

描述（由申请人提供）：线虫秀丽隐杆线虫中前后（A-P）身体轴的极化发生在受精后不久和第一轮有丝分裂之前。卵母细胞染色体结束后，这种极化事件是密切连续的。有趣的是，尽管已经确定了很少的精子供供供因子，但减数分裂的完成和轴极化都是由精子的线索触发的。最近的研究表明，减数分裂出口缺陷通常与轴心建立中的缺陷相关，这表明这两个过程可能在发展上是联系的。尽管如此，关于这些事件如何在单元格中的时间或两者之间可能的相互作用的情况下，知之甚少。为了研究这个问题，将在秀丽隐杆线虫中研究SCU-1（精子提示异常）基因。 SCU-1中的突变导致减数分裂出口缺陷和未能使A-P轴极化。此外，SCU-1基因产物在母体和亲子阶层都得到贡献，这可能会使人们对亲子融合提供的蛋白质有更好的了解。 为了揭示SCU-1调节大规模出口和轴极化的机制，研究将重点放在三个特定目标上。 1）SCU-1在减数分裂出口期间的作用将通过测试MAPK中SCU-1的作用，并在减数分裂后失活的MPF，并解剖SCU-1在减数分裂过程中的母亲和父亲的贡献。 2）SCU-1基因的分子认同和蛋白质的亚细胞定位将通过分子克隆和抗体产生和染色确定3）SCU-1相互作用的蛋白质将通过遗传抑制筛选和全基因组RNA Interperion而鉴定屏幕增强剂。这些研究应提供有关控制早期胚胎细胞周期和极性协调的机制的见解。