Abstract
ERK3 (extracellular signal-regulated kinase 3) is an atypical member of the mitogen-activated protein (MAP) kinase family of serine/threonine kinases. Little is known about its function in mitosis, and even less about its roles in mammalian oocyte meiosis. In the present study, we examined the localization, expression and functions of ERK3 during mouse oocyte meiotic maturation. Immunofluorescent analysis showed that ERK3 localized to the spindles from the pre-MI stage to the MII stage. ERK3 co-localized with α-tubulin on the spindle fibers and asters in oocytes after taxol treatment. Deletion of ERK3 by microinjection of ERK3 morpholino (ERK3 MO) resulted in oocyte arrest at the MI stage with severely impaired spindles and misaligned chromosomes. Most importantly, the spindle assembly checkpoint protein BubR1 could be detected on kinetochores even in oocytes cultured for 10 h. Low temperature treatment experiments indicated that ERK3 deletion disrupted kinetochore-microtubule (K-MT) attachments. Chromosome spreading experiments showed that knock-down of ERK3 prevented the segregation of homologous chromosomes. Our data suggest that ERK3 is crucial for spindle stability and required for the metaphase-anaphase transition in mouse oocyte maturation.
Highlights
In mammalian oocytes, synapsis and meiotic recombination occur during fetal development, after which the oocyte enters prophase I arrest, or diplotene arrest
Extracellular signal-regulated kinase 3 (ERK3) mainly distributed in the germinal vesicle at the GV stage
Most studies on ERK3 focus on its functions in mitosis, and ERK3-deficient mice have been found to have neonatal lethality[20]; we want to dig up the function of ERK3 in meiosis, especially during mouse oocyte meiotic maturation
Summary
Synapsis and meiotic recombination occur during fetal development, after which the oocyte enters prophase I arrest, or diplotene arrest. Gly sequence instead of conserved Thr-Xaa-Tyr motif in the activation loop and ERK3 has a unique C-terminal extension terminal of 178 amino acids, which is demonstrated to link its stability[14,15]. Benjamin and his colleagues reported cloning and characterization of the mouse ERK3 gene[16]. Our results indicated that ERK3 deletion arrested oocyte maturation at the MI stage by disrupting the attachment between kinetochores and microtubules and activating the SAC component BubR1. The results provide evidence to show that ERK3 is required for spindle stability and metaphase-anaphase transition during mouse oocyte maturation
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
