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 paradigm 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. At a molecular level, the oocyte responses apparently involve the control of conserved protein kinase pathways and post-transcriptional gene regulation in the oocyte. At a cellular level, the responses include cortical cytoskeletal rearrangement, nuclear envelope breakdown, assembly of the acentriolar meiotic spindle, chromosome segregation, and likely changes important for fertilization and the oocyte-to-embryo transition. This chapter focuses on signaling mechanisms required for oocyte growth and meiotic maturation in C. elegans and discusses how these mechanisms coordinate the completion of meiosis and the oocyte-to-embryo transition.
|Original language||English (US)|
|Title of host publication||Germ Cell Development in C. elegans|
|Publisher||Springer Science and Business Media, LLC|
|Number of pages||44|
|State||Published - 2013|
|Name||Advances in Experimental Medicine and Biology|
Bibliographical noteFunding Information:
We are grateful to Valerie Osterberg, Sara Christensen, and Bruce Bowerman for providing Fig. a. Thanks to Swathi Arur, Bruce Bowerman, Andy Golden, Frank McNally, Michael Miller, Martin Srayko, and Jennifer Schisa for providing comments on the manuscript. Thanks to Bruce Bowerman, Amaranath Govindan, Tim Schedl, Jennifer Schisa, and Todd Starich for communication of unpublished results. This work was supported by NIH grants GM65115 and GM57173 to D.G.
- G-protein signaling
- Major sperm protein
- Meiotic chromosome segregation
- Meiotic maturation signaling
- Meiotic resumption
- Meiotic spindle