Peroxiredoxins are required for spindle assembly, chromosome organization, and polarization in mouse oocytes

Peroxiredoxins (Prxs) are highly conserved antioxidant enzymes and are implicated in multiple biological processes; however, their function in oocyte meiosis has not been studied. Here we show that inhibition of Prx I and II results in spindle defects, chromosome disorganization, and impaired polari...

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Published in:Biochemical and biophysical research communications Vol. 489; no. 2; pp. 193 - 199
Main Authors: Jeon, Hyuk-Joon, Park, Yong Seok, Cho, Dong-Hyung, Kim, Jae-Sung, Kim, Eunji, Chae, Ho Zoon, Chun, Sang-Young, Oh, Jeong Su
Format: Journal Article
Language:English
Published: United States Elsevier Inc 22-07-2017
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Summary:Peroxiredoxins (Prxs) are highly conserved antioxidant enzymes and are implicated in multiple biological processes; however, their function in oocyte meiosis has not been studied. Here we show that inhibition of Prx I and II results in spindle defects, chromosome disorganization, and impaired polarization in mouse oocytes. Prx I was specifically localized at the spindle, whereas Prx II was enriched at the oocyte cortex and chromosomes. Inhibition of Prx activity with conoidin A disturbed assembly of the microtubule organizing center (MTOC) through Aurora A regulation, leading to defects in spindle formation. Moreover, conoidin A impaired actin filament and cortical granule (CG) distribution, disrupting actin cap and CG formation, respectively. Conoidin A also increased DNA damage without significantly increasing reactive oxygen species (ROS) levels, suggesting that the effects of conoidin A on meiotic maturation are not likely associated with ROS scavenging pathways. Therefore, our data suggest that Prxs are required for spindle assembly, chromosome organization, and polarization during meiotic maturation. •Conoidin A disturbs spindle assembly and chromosome organization.•Conoidin A disrupts MTOC organization via Aurora A dysregulation.•Conoidin A impairs polarization of oocytes without changing cellular ROS level.
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ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2017.05.127