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Updated: Sep 24, 2026

Meiotic Spindle Assessment in Mouse Oocytes by siRNA-mediated Silencing
Published on: October 11, 2015
The spindle-associated antisense RNA ARHGEF17-AS1 functionally contributes to mitotic spindle integrity
Sagar Mahale1, Meenakshi Setia1, Daniel Sjövall2
1Department of Medical Biochemistry and Cell Biology, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, 40530 Gothenburg, Sweden.
Abstract:
Long non-coding RNAs (lncRNAs) are increasingly recognized as regulators of mitotic progression, yet few have been shown to act directly at the mitotic spindle. Here we identify ARHGEF17-AS1 as a metaphase-enriched antisense RNA that localizes to the mitotic spindle and is associated with spindle pole integrity. ARHGEF17-AS1 interacts with RPS3 and the dynein motor complex and is associated with RPS3 recruitment to the mitotic spindle and with the RPS3-dynein interaction. Depletion of ARHGEF17-AS1 reduces this interaction and decreases RPS3 accumulation at spindle poles. ARHGEF17-AS1 depletion is also associated with lower RPS3 abundance, reduced RNF10 expression, and loss of mitosis-associated RPS3 monoubiquitination at lysine 214. These perturbations coincide with altered spindle microtubule organization and delayed mitotic progression. Together, the data support a model in which ARHGEF17-AS1 contributes to spindle organization through an RNA-mediated pathway involving extra-ribosomal RPS3, dynein, and RNF10, supporting an important role for ARHGEF17-AS1 in mitotic spindle organization.
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