Abstract
BackgroundRal family is a member of Ras-like GTPase superfamily, which includes RalA and RalB. RalA/B play important roles in many cell biological functions, including cytoskeleton dynamics, cell division, membrane transport, gene expression and signal transduction. However, whether RalA/B involve into the mammalian oocyte meiosis is still unclear. This study aimed to explore the roles of RalA/B during mouse oocyte maturation.ResultsOur results showed that RalA/B expressed at all stages of oocyte maturation, and they were enriched at the spindle periphery area after meiosis resumption. The injection of RalA/B siRNAs into the oocytes significantly disturbed the polar body extrusion, indicating the essential roles of RalA/B for oocyte maturation. We observed that in the RalA/B knockdown oocytes the actin filament fluorescence intensity was significantly increased at the both cortex and cytoplasm, and the chromosomes were failed to locate near the cortex, indicating that RalA/B regulate actin dynamics for spindle migration in mouse oocytes. Moreover, we also found that the Golgi apparatus distribution at the spindle periphery was disturbed after RalA/B depletion.ConclusionsIn summary, our results indicated that RalA/B affect actin dynamics for chromosome positioning and Golgi apparatus distribution in mouse oocytes.
Highlights
Ral family is a member of Ras-like GTPase superfamily, which includes RalA and RalB
Our results showed that the perturbation of RalA/B affected chromosome positioning and Golgi apparatus distribution by regulating actin dynamics, which further led to the failure of polar body extrusion during mouse oocyte meiosis
When oocytes were in the metaphase I (MI) and metaphase II (MII) stages, RalA/B were mainly distributed around the spindle
Summary
Ral family is a member of Ras-like GTPase superfamily, which includes RalA and RalB. RalA/B play important roles in many cell biological functions, including cytoskeleton dynamics, cell division, membrane transport, gene expression and signal transduction. Arp2/3 complex is reported to involve into actin-mediated spindle migration to the oocyte cortex [38]; while Formin 2 deficiency caused the central-arrested chromosomes in mouse oocytes [19]. Other formin subfamilies such as mDia, Formin like 1 (FMNL1), FMNL3 and FHOD1 are shown to affect actin assembly or distribution for spindle migration in mouse oocytes [28, 29, 47]. Rho GTPase RhoA-mediated ROCK-LIMK pathway and Arf GTPase Arf are shown to affect Arp2/3 complex or cofilin for actin assembly/disassembly in mammalian oocytes [6,7,8]
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