title: Regulation of asymmetrical cytokinesis by cAMP during meiosis I in mouse oocytes.
abstract: Mammalian oocytes undergo an asymmetrical first meiotic division, extruding half of their chromosomes in a small polar body to preserve maternal resources for embryonic development. To divide asymmetrically, mammalian oocytes relocate chromosomes from the center of the cell to the cortex, but little is known about the underlying mechanisms. Here, we show that upon the elevation of intracellular cAMP level, mouse oocytes produced two daughter cells with similar sizes. This symmetrical cell division could be rescued by the inhibition of PKA, a cAMP-dependent protein kinase. Live cell imaging revealed that a symmetrically localized cleavage furrow resulted in symmetrical cell division. Detailed analyses demonstrated that symmetrically localized cleavage furrows were caused by the inappropriate central positioning of chromosome clusters at anaphase onset, indicating that chromosome cluster migration was impaired. Notably, high intracellular cAMP reduced myosin II activity, and the microinjection of phospho-myosin II antibody into the oocytes impeded chromosome migration and promoted symmetrical cell division. Our results support the hypothesis that cAMP plays a role in regulating asymmetrical cell division by modulating myosin II activity during mouse oocyte meiosis I, providing a novel insight into the regulation of female gamete formation in mammals.
authors.affiliation: School of Life Sciences, University of Science and Technology of China, Hefei, China.
authors.forename: Dawei
authors.initials: D
authors.lastname: Chen
authors.forename: Yuanwei
authors.initials: Y
authors.lastname: Zhang
authors.forename: Qiyi
authors.initials: Q
authors.lastname: Yi
authors.forename: Yun
authors.initials: Y
authors.lastname: Huang
authors.forename: Heli
authors.initials: H
authors.lastname: Hou
authors.forename: Yingyin
authors.initials: Y
authors.lastname: Zhang
authors.forename: Qiaomei
authors.initials: Q
authors.lastname: Hao
authors.forename: Howard J
authors.initials: HJ
authors.lastname: Cooke
authors.forename: Lei
authors.initials: L
authors.lastname: Li
authors.forename: Qingyuan
authors.initials: Q
authors.lastname: Sun
authors.forename: Qinghua
authors.initials: Q
authors.lastname: Shi
mesh_terms: D015056:1-Methyl-3-isobutylxanthine / Q000494:pharmacology; D000705:Anaphase / Q000187:drug effects; D000818:Animals; D060049:Asymmetric Cell Division / Q000187:drug effects*; D003994:Bucladesine / Q000494:pharmacology; D002465:Cell Movement / Q000187:drug effects; D002478:Cells, Cultured; D033481:Chromosomes, Mammalian / Q000378:metabolism; D000242:Cyclic AMP / Q000494:pharmacology*; D048749:Cytokinesis / Q000187:drug effects*; D005260:Female; D042541:Intracellular Space / Q000187:drug effects / Q000378:metabolism; D007546:Isoquinolines / Q000494:pharmacology; D008540:Meiosis / Q000187:drug effects*; D051379:Mice; D008813:Mice, Inbred ICR; D008845:Microinjections; D024462:Myosin Type II / Q000378:metabolism; D009865:Oocytes / Q000166:cytology* / Q000187:drug effects*; D013449:Sulfonamides / Q000494:pharmacology
chemical_list: D007546:Isoquinolines; D013449:Sulfonamides; D003994:Bucladesine; D000242:Cyclic AMP; D024462:Myosin Type II; C063509:N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide; D015056:1-Methyl-3-isobutylxanthine