RAB35 depletion affects spindle formation and actin-based spindle migration in mouse oocyte meiosis.

Autor: Zhang Y; College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China., Wan X; College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China., Wang HH; College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China., Pan MH; College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China., Pan ZN; College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China., Sun SC; College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China.
Jazyk: angličtina
Zdroj: Molecular human reproduction [Mol Hum Reprod] 2019 Jul 01; Vol. 25 (7), pp. 359-372.
DOI: 10.1093/molehr/gaz027
Abstrakt: Mammalian oocyte maturation involves a unique asymmetric cell division, in which meiotic spindle formation and actin filament-mediated spindle migration to the oocyte cortex are key processes. Here, we report that the vesicle trafficking regulator, RAB35 GTPase, is involved in regulating cytoskeleton dynamics in mouse oocytes. RAB35 GTPase mainly accumulated at the meiotic spindle periphery and cortex during oocyte meiosis. Depletion of RAB35 by morpholino microinjection led to aberrant polar body extrusion and asymmetric division defects in almost half the treated oocytes. We also found that RAB35 affected SIRT2 and αTAT for tubulin acetylation, which further modulated microtubule stability and meiotic spindle formation. Additionally, we found that RAB35 associated with RHOA in oocytes and modulated the ROCK-cofilin pathway for actin assembly, which further facilitated spindle migration for oocyte asymmetric division. Importantly, microinjection of Myc-Rab35 cRNA into RAB35-depleted oocytes could significantly rescue these defects. In summary, our results suggest that RAB35 GTPase has multiple roles in spindle stability and actin-mediated spindle migration in mouse oocyte meiosis.
(© The Author(s) 2019. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)
Databáze: MEDLINE