scholarly journals Exogenous thymine DNA glycosylase regulates epigenetic modifications and meiotic cell cycle progression of mouse oocytes

2014 ◽  
Vol 21 (2) ◽  
pp. 186-194 ◽  
Author(s):  
Jun-Yu Ma ◽  
Kun Zhao ◽  
Ying-Chun OuYang ◽  
Zhen-Bo Wang ◽  
Yi-Bo Luo ◽  
...  
2018 ◽  
Vol 9 (1) ◽  
Author(s):  
Qian-Qian Sha ◽  
Xing-Xing Dai ◽  
Jun-Chao Jiang ◽  
Chao Yu ◽  
Yu Jiang ◽  
...  

Development ◽  
2016 ◽  
Vol 144 (3) ◽  
pp. 452-463 ◽  
Author(s):  
Qian-Qian Sha ◽  
Xing-Xing Dai ◽  
Yujiao Dang ◽  
Fuchou Tang ◽  
Junping Liu ◽  
...  

10.1038/10100 ◽  
1999 ◽  
Vol 1 (2) ◽  
pp. 127-129 ◽  
Author(s):  
Jochen Scheel ◽  
Jagan Srinivasan ◽  
Ulrike Honnert ◽  
Annemarie Henske ◽  
Teymuras V. Kurzchalia

2018 ◽  
Vol 37 (24) ◽  
Author(s):  
Qian‐Qian Sha ◽  
Jia‐Li Yu ◽  
Jing‐Xin Guo ◽  
Xing‐Xing Dai ◽  
Jun‐Chao Jiang ◽  
...  

Development ◽  
1995 ◽  
Vol 121 (8) ◽  
pp. 2525-2535 ◽  
Author(s):  
D.L. Church ◽  
K.L. Guan ◽  
E.J. Lambie

In the germline of Caenorhabditis elegans hermaphrodites, meiotic cell cycle progression occurs in spatially restricted regions. Immediately after leaving the distal mitotic region, germ cells enter meiosis and thereafter remain in the pachytene stage of first meiotic prophase for an extended period. At the dorsoventral gonadal flexure, germ cells exit pachytene and subsequently become arrested in diakinesis. We have found that exit from pachytene is dependent on the function of three members of the MAP kinase signaling cascade. One of these genes, mek-2, is a newly identified C. elegans MEK (MAP kinase kinase). The other two genes, mpk-1/sur-1 (MAP kinase) and let-60 ras, were previously identified based on their roles in vulval induction and are shown here to act in combination with mek-2 to permit exit from pachytene. Through genetic mosaic analysis, we demonstrate that the expression of mpk-1/sur-1 is required within the germline to permit exit from pachytene.


Zygote ◽  
2003 ◽  
Vol 11 (4) ◽  
pp. 329-337 ◽  
Author(s):  
He-Mei Quan ◽  
Heng-Yu Fan ◽  
Xiao-Qian Meng ◽  
Li-Jun Huo ◽  
Da-Yuan Chen ◽  
...  

Protein kinase C (PKC) is a family of Ser/Thr protein kinase widely distributed in eukaryotes. There is evidence that PKC plays key roles in the meiotic maturation and activation of mammalian oocytes. However, the mechanism of PKC's actions and the PKC isoforms responsible for these actions are poorly understood. In this study, we reveal in mouse eggs and early embryos: (1) the effects of PKC on the meiotic and mitotic cell cycle progression during oocyte maturation, egg activation and embryonic cleavages; (2) the functional importance of classical PKC subclasses in these processes; and (3) the subcellular localization of the PKCα isoform during development from GV stage oocytes to the blastocyst stage embryos. The results indicate that the PKC activator phorbol 12-myristate 13-acetate (PMA) inhibits the meiotic resumption of cumulus-free mouse oocytes by a mechanism dependent not only on classical PKC activity but also on other PKC isoforms. PKC activation after germinal vesicle breakdown leads to the inhibition of mitogen-activated protein kinase phosphorylation and the arrest of cell cycle at MI stage. The second polar body emission and the cleavages of early embryos are blocked after prolonged PKC activation. The subcellular localization of PKCα isoform in mouse oocytes and embryos is developmental-stage associated. All these results suggest that PKC has multiple functional roles in the cell cycle progression of mouse oocytes and embryos.


2020 ◽  
Vol 34 (3-4) ◽  
pp. 166-178
Author(s):  
Chunxia Zhang ◽  
Zhiyuan Chen ◽  
Qiangzong Yin ◽  
Xudong Fu ◽  
Yisi Li ◽  
...  

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