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On the genetic control of oocyte meiotic maturation in Caenorhabditis elegans.

机译：关于秀丽隐杆线虫卵母细胞减数分裂成熟的遗传控制。

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摘要

In sexually reproducing animals, oocytes arrest at diplotene or diakinesis and resume meiosis (meiotic maturation) in response to hormones. Chromosome segregation errors in female meiosis I are the leading cause of human birth defects, and age-related changes in the hormonal environment of the ovary are a suggested cause. Caenorhabditis elegans is emerging as a genetic system for studying hormonal control of meiotic maturation. The meiotic maturation processes in C. elegans and mammals share a number of biological and molecular similarities. Major sperm protein (MSP) and luteinizing hormone (LH), though unrelated in sequence, both trigger meiotic resumption using somatic Gαs-adenylate cyclase pathways and soma-germline gap-junctional communication. I used C. elegans as a model for studying the genetic control of oocyte meiotic maturation. I conducted a forward genetic screen to identify new regulators of meiotic maturation that function downstream of somatic Gαs-adenylate cyclase signaling. I screened for mutations that suppress the meiotic maturation defect caused by defective Gαs-adenylate cyclase signaling and identified ten Sacy (s&barbelow;uppressor of acy-4 sterility) genetic loci, including sacy-1, which encodes a highly conserved DEAD-box helicase. SACY-1 appears to be a multifunctional protein that establishes a mechanistic link connecting the somatic control of meiotic maturation to germline sex determination, gamete maintenance, and post-transcriptional gene regulation in the germ line.;To identify the molecular mechanisms by which sacy-1 functions in multiple germline developmental pathways, I conducted a genome-wide RNAi screen for genetic loci that enhance a hypomorphic sacy-1 mutant allele upon their depletion. This RNAi enhancer screen revealed multiple spliceosomal C complex proteins as genetic interactors of sacy-1. This result suggests several potential models for future work. One possibility is that sacy-1 might function as a spliceosomal component to regulate specific splicing events needed for execution of multiple germline developmental events. Alternatively, sacy-1, together with a subset of spliceosomal C complex components, might regulate downstream protein-RNA transactions important for germline development. While my work provides insights gained from a genetic analysis of meiotic maturation signaling in C. elegans, the conserved factors identified here might inform analysis in other systems through either homology or analogy.
机译：在有性繁殖的动物中，卵母细胞停滞在二戊烯或双反应性，并响应激素而恢复减数分裂（减数分裂成熟）。女性减数分裂I中的染色体分离错误是人类出生缺陷的主要原因，而卵巢激素环境中与年龄相关的变化则是可能的原因。秀丽隐杆线虫（Caenorhabditis elegans）逐渐成为研究激素控制减数分裂成熟的遗传系统。秀丽隐杆线虫和哺乳动物的减数分裂成熟过程具有许多生物学和分子相似性。主要精子蛋白（MSP）和促黄体生成激素（LH）尽管顺序不相关，但两者均通过体细胞Gαs-腺苷酸环化酶途径和体细胞-种系间隙连接交流触发减数分裂恢复。我用秀丽隐杆线虫作为模型研究卵母细胞减数分裂成熟的遗传控制。我进行了正向遗传筛选，以鉴定在体细胞Gαs-腺苷酸环化酶信号传导下游起作用的减数分裂成熟的新调控因子。我筛选了可抑制由有缺陷的Gαs-腺苷酸环化酶信号转导引起的减数分裂成熟缺陷的突变，并鉴定了10个Sacy（acy-4不育的抑制子）基因位点，包括sacy-1，它编码高度保守的DEAD-box解旋酶。 SACY-1似乎是一种多功能蛋白，它建立了将减数分裂成熟的体细胞控制与种系性别确定，配子维持以及种系中转录后基因调控联系起来的机制链接。 1在多种种系发育途径中起作用，我进行了基因组范围的全基因组RNAi筛查，以寻找可减少缺失的sacy-1突变等位基因的基因座。该RNAi增强子筛选揭示了多个剪接体C复合蛋白作为sacy-1的遗传相互作用因子。这一结果为未来的工作提出了几种潜在的模型。一种可能性是sacy-1可能作为剪接体组件来调节执行多个种系发育事件所需的特定剪接事件。或者，sacy-1与剪接体C复合物组分的子集一起，可能会调节对于种系发育很重要的下游蛋白质RNA交易。虽然我的工作提供了从秀丽隐杆线虫减数分裂成熟信号转导的遗传分析中获得的见识，但此处确定的保守因素可能通过同源性或类比为其他系统的分析提供了信息。

著录项

  • 作者

    Kim, Seongseop.;

  • 作者单位

    University of Minnesota.;

  • 授予单位 University of Minnesota.;
  • 学科 Biology Genetics.;Health Sciences Human Development.
  • 学位 Ph.D.
  • 年度 2013
  • 页码 252 p.
  • 总页数 252
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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