Rab32-based vesicles coordinate mitochondria and actin for spindle migration and organelle rearrangement in oocyte meiosis
- PMID: 40324632
- DOI: 10.1016/j.jare.2025.05.001
Rab32-based vesicles coordinate mitochondria and actin for spindle migration and organelle rearrangement in oocyte meiosis
Abstract
Introduction: Rab32 is a part of the Rab GTPase family, which is known as the regulator of vesicle transport for an array of cellular functions including endosomal transport, autophagy, generation of melanosomes, phagocytosis and inflammatory processes.
Objective: However, the role of Rab32 in oocyte meiosis is still not well-defined.
Methods: We depleted Rab32 expression by knock down approach, and we also disrupted Rab32 function by exogenous Rab32Q83L/T37N mRNA injection for mutation.
Results: In our current investigation, we delved into its impacts on the cytoskeleton dynamics and the functionality of organelles during the meiotic maturation process in mouse oocytes. Rab32 expressed during oocyte meiosis and deletion of Rab32 or the expression of exogenous Rab32Q83L/T37N led to oocyte polar body extrusion defects or symmetric division. We showed that Rab32 was essential for ROCK1-based actin assembly which further led to spindle migration for the asymmetry. Besides, perturbation of Rab32 affected DRP1 phosphorylation for the spatial arrangement and functionality of mitochondria in mouse oocytes. And we found that Rab32 disruption caused the miscarriage of membrane organelles such as Golgi apparatus, ER, lysosome and CGs during oocyte meiosis, leading to ER stress and autophagy.
Conclusions: In summary, our study unravels the critical functions of Rab32 for the interplay between actin and mitochondria, which further facilitates movement of the spindle apparatus and organelles arrangement in mouse oocyte meiotic development.
Keywords: Actin; Meiosis; Mitochondria; Organelles; Rab32.
Copyright © 2025 The Author(s). Published by Elsevier B.V. All rights reserved.
Conflict of interest statement
Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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