4.6 Article

GTPases Arf5 and Arl2 function partially distinctly during oocyte meiosis

Journal

JOURNAL OF CELLULAR BIOCHEMISTRY
Volume 122, Issue 2, Pages 198-208

Publisher

WILEY
DOI: 10.1002/jcb.29839

Keywords

Arf5; Arl2; GTPase; meiosis; mouse; oocyte

Funding

  1. General Program of the National Natural Science Foundation of China [31671561]
  2. Natural Science Research Project of Universities in Jiangsu Province [18KJD180001]
  3. Science and Technology Development Fund of Nanjing Medical University [NMUB2018044]
  4. Youth Program of National Natural Science Foundation of China [81901474]

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Arl2 and Arf5 are two novel essential GTPases in mouse oocytes, and their depletion impairs meiotic progression by affecting spindles and microfilaments, respectively. Depletion of Arl2 and Arf5 also leads to increased reactive oxygen species levels and decreased mitochondrial membrane potential and autophagy, ultimately damaging oocyte quality.
Mammalian female meiosis must be tightly regulated to produce high-quality mature oocytes for subsequent regular fertilization and healthy live birth of the next generation. GTPases control many important signal pathways involved in diverse cellular activities. ADP-ribosylation factor family members (Arfs) in mice possess GTPase activities, and some members have been found to function in meiosis. However, whether other Arfs play a role in meiosis is unknown. In this study, we found that Arl2 and Arf5 are the richest among Arfs in mouse oocytes, and they are more abundant in oocytes than in granular cells. Furthermore, Arl2 and Arf5 depletion both impeded meiotic progression, but by affecting spindles and microfilaments, respectively. Moreover, Arl2 and Arf5 depletion both significantly increased regular reactive oxygen species levels and decreased mitochondrial membrane potential and autophagy, indicating that oocyte quality was damaged by Arl2 and Arf5 depletion. These results suggest that Arl2 and Arf5 are two novel essential GTPases required for oocyte meiosis and quality control.

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