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    Home > Biochemistry News > Biotechnology News > Cyclin B2 compensates ForCyclin B1 to regulate the new mechanism of subtraction division.

    Cyclin B2 compensates ForCyclin B1 to regulate the new mechanism of subtraction division.

    • Last Update: 2020-08-08
    • Source: Internet
    • Author: User
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    In mammals, oocytes are blocked for months or even years before the first subtraction, depending on the species.
    fully developed oocytes to resume subtraction and division require splintering mpF factors (Phase M promoters), which are made up of Cyclin B1 and CDK1 (cell cycle-dependent kinase 1).
    , the synthesis and accumulation of Cyclin B1 and its interaction with CDK1 have long been considered to be a prerequisite for oocytes to activate MPF, thus restoring the reduction of oocyte division.
    researchers at the Institute of Zoology of the Chinese Academy of Sciences, Liu Yitao, found that in the absence of Cyclin B1, oocyte reduction division can still be restored and discharged from the first pole.
    the female mice that were knocked out by Cyclin B1 were infertile, mainly because MPF activity could not rise rapidly during the transition at the end of the first division of the minus and the second division of the reduction, and the oocytes entered a mesoperiod block after the end of the reduction first division.
    in the case of knocking out Cyclin B1, CDK1 can be activated by the uplifted Cyclin B2, pushing the reduction to the first split.
    when Cyclin B1 and Cyclin B2 are knocked out simultaneously in the oocytes, the oocytes are completely blocked in the early stages of the first subtraction.
    these results reveal that oocytes hide important compensation mechanisms between Cyclin B1 and Cyclin B2 during the process of regulating MPF and subtracted division.
    the study was published in the journal of Cell Biology. Li Jian, a doctoral student in
    , is the first author of the thesis, Tang Jixin is the first author, and Liu Yichen is the communication author of the thesis.
    the research was supported by the National Natural Science Foundation of China, the Ministry of Science and Technology of the People's Republic of China and the Beijing Natural Science Foundation.
    Source: Animal Research Institute.
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