Effects of puberty and gonadotropins on the molecular events controlling meiotic resumption of mouse oocytes.
Although studies suggest that the low competence of oocytes from prepubertal animals is due to their insufficient cytoplasmic maturation and that FSH improves oocyte maturation possibly by retarding meiotic progression and allowing more time for cytoplasmic maturation, the mechanisms by which puberty and gonadotropins regulate meiotic progression require additional detailed studies. For the first time, we observed that while meiotic progression was significantly slower, the maturation-promoting factor (MPF) activity of oocytes was significantly higher in prepubertal than in adult mice. To resolve this contradiction, we specified the molecules regulating the MPF activity and their localization during oocyte maturation in prepubertal and adult mice primed with or without gonadotropins. Our tests using corresponding enzyme regulators suggested that while activities of protein kinase A were unaffected, the activity of adenylate cyclase (ADCY) and phosphodiesterase increased while cell division cycle 2 homolog A (CDC2A) decreased significantly after puberty. While most of the adult oocytes had CDC2A protein concentrated in the germinal vesicle (GV) region, the majority of prepubertal oocytes showed no nuclear concentration of CDC2A. Maximally priming mice with equine chorionic gonadotropin brought the above parameters of prepubertal oocytes close to those in adult oocytes. Together, the results suggest that puberty and gonadotropin control oocyte meiotic progression mainly by regulating the ADCY activity and the concentration of the activated MPF toward the GV region.
Han
Dong
D
Laboratory for Animal Reproduction and Embryology, College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai-an City 271018, Shandong Province, People's Republic of China.
Cao
Xin-Yan
XY
Wang
Hui-Li
HL
Li
Jing-Jing
JJ
Wang
Yan-Bo
YB
Tan
Jing-He
JH
D000262:Adenylyl Cyclases / Q000378:metabolism; D000818:Animals; D016203:CDC2 Protein Kinase / Q000032:analysis; D017868:Cyclic AMP-Dependent Protein Kinases / Q000378:metabolism; D003593:Cytoplasm / Q000502:physiology; D005260:Female; D006062:Gonadotropins / Q000008:administration & dosage / Q000502:physiology*; D006064:Gonadotropins, Equine / Q000008:administration & dosage; D047908:Intracellular Signaling Peptides and Proteins / Q000502:physiology; D016200:Maturation-Promoting Factor / Q000502:physiology; D008540:Meiosis / Q000502:physiology*; D000090204:Mesothelin; D051379:Mice; D009865:Oocytes / Q000502:physiology* / Q000648:ultrastructure; D010727:Phosphoric Diester Hydrolases / Q000378:metabolism; D011494:Protein Kinases / Q000378:metabolism; D012741:Sexual Maturation / Q000502:physiology*
D006062:Gonadotropins; D006064:Gonadotropins, Equine; D047908:Intracellular Signaling Peptides and Proteins; C000715528:Msln protein, mouse; D011494:Protein Kinases; C102333:histone H1 kinase; D017868:Cyclic AMP-Dependent Protein Kinases; D016203:CDC2 Protein Kinase; D016200:Maturation-Promoting Factor; D010727:Phosphoric Diester Hydrolases; D000262:Adenylyl Cyclases; D000090204:Mesothelin