Kim, Seongseop2013-07-232013-07-232013-05https://hdl.handle.net/11299/153665University of Minnesota Ph.D. dissertation. May 2013. Major: Molecular, Cellular, Developmental Biology and Genetics. Advisor: David I. Greenstein. 1 computer file (PDF); ix, 238 pages.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 Gαadenylate 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 Gαadenylate cyclase signaling. I screened for mutations that suppress the meiotic maturation defect caused by defective Gαadenylate cyclase signaling and identified ten Sacy of underline acy underline-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.en-USC. elegansG protein signalingMeiosisOocyteSacy-1SpliceosomeThesis or Dissertation