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首页> 外文期刊>Cell cycle >Female infertility in PDE3A(-/-) mice: polo-like kinase 1 (Plk1) may be a target of protein kinase A (PKA) and involved in meiotic arrest of oocytes from PDE3A(-/-) mice.
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Female infertility in PDE3A(-/-) mice: polo-like kinase 1 (Plk1) may be a target of protein kinase A (PKA) and involved in meiotic arrest of oocytes from PDE3A(-/-) mice.

机译：PDE3A（-/-）小鼠中的女性不育：polo样激酶1（Plk1）可能是蛋白激酶A（PKA）的靶标，并参与了PDE3A（-/-）小鼠卵母细胞的减数分裂。

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Mechanisms of cAMP/PKA-induced meiotic arrest in oocytes are not completely identified. In cultured, G2/M-arrested PDE3A(-/-) murine oocytes, elevated PKA activity was associated with inactivation of Cdc2 and Plk1, and inhibition of phosphorylation of histone H3 (S10) and of dephosphorylation of Cdc25B (S323) and Cdc2 (Thr14/Tyr15). In cultured WT oocytes, PKA activity was transiently reduced and then increased to that observed in PDE3A(-/-) oocytes; Cdc2 and Plk1 were activated, phosphorylation of histone H3 (S10) and dephosphorylation of Cdc25B (S323) and Cdc2 (Thr14/Tyr15) were observed. In WT oocytes, PKAc were rapidly translocated into nucleus, and then to the spindle apparatus, but in PDE3A(-/-) oocytes, PKAc remained in the cytosol. Plk1 was reactivated by incubation of PDE3A(-/-) oocytes with PKA inhibitor, Rp-cAMPS. PDE3A was co-localized with Plk1 in WT oocytes, and co-immunoprecipitated with Plk1 in WT ovary and Hela cells. PKAc phosphorylated rPlk1 and Hela cell Plk1 and inhibited Plk1 activity in vitro. Our results suggest that PKA-induced inhibition of Plk1 may be critical in oocyte meiotic arrest and female infertility in PDE3A(-/-) mice.
机译：cAMP / PKA诱导卵母细胞减数分裂停滞的机制尚未完全确定。在培养的G2 / M逮捕的PDE3A（-/-）鼠卵母细胞中，升高的PKA活性与Cdc2和Plk1的失活，组蛋白H3（S10）的磷酸化以及Cdc25B（S323）和Cdc2的去磷酸化的抑制有关（ Thr14 / Tyr15）。在培养的WT卵母细胞中，PKA活性暂时降低，然后增加到PDE3A（-/-）卵母细胞中观察到的活性; Cdc2和Plk1被激活，观察到组蛋白H3（S10）的磷酸化以及Cdc25B（S323）和Cdc2（Thr14 / Tyr15）的去磷酸化。在WT卵母细胞中，PKAc迅速转移到细胞核中，然后转移到纺锤体中，但是在PDE3A（-/-）卵母细胞中，PKAc保留在细胞质中。通过与PKA抑制剂Rp-cAMPS孵育PDE3A（-/-）卵母细胞来重新激活Plk1。 PDE3A与Plk1在WT卵母细胞中共定位，并与Plk1在WT卵巢和Hela细胞中共免疫沉淀。 PKAc磷酸化rPlk1和Hela细胞Plk1，并在体外抑制Plk1活性。我们的结果表明，PKA诱导的Plk1抑制可能对PDE3A（-/-）小鼠的卵母细胞减数分裂阻滞和女性不育至关重要。

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