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首页> 外文期刊>Cell and Tissue Research >Decreased cyclin-dependent kinase activity promotes thyroid hormone-dependent tail regression in Rana catesbeiana
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Decreased cyclin-dependent kinase activity promotes thyroid hormone-dependent tail regression in Rana catesbeiana

机译：细胞周期蛋白依赖性激酶活性的降低促进了蛙蛙的甲状腺激素依赖性尾巴消退

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The thyroid hormone (TH), 3,5,3′-triiodothyronine (T3), is an important regulator of diverse cellular processes including cell proliferation, differentiation, and apoptosis, with increasing evidence that the modulation of the phosphoproteome is an important factor in the TH-mediated response. However, little is understood regarding the mechanisms whereby phosphorylation may contribute to T3-mediated cellular outcomes during development. The cyclin-dependent kinases (Cdks) and mitogen-activated protein kinases (MAPK/ERK) have been implicated in TH signaling in mammalian cells. In this study, we have investigated, in frogs, the possible role that these kinases may have in the promotion of tail regression during tadpole metamorphosis, an important postembryonic process that is completely TH-dependent. Cdk2 steady state levels and activity increase in the tail concurrent with progression through the growth phase of metamorphosis, followed by a precipitous decrease coinciding with tail regression. Cyclin-A-associated kinase activity also follows a similar trend except that its associated kinase activity is maintained longer before a decrease in activity. Protein steady state levels of ERK1 and ERK2 remain relatively constant, and their kinase activities do not decrease until much later during tail regression. Tail tips cultured in serum-free medium in the presence of T3 undergo regression, which is accelerated by coincubation with a specific Cdk2 inhibitor. Coincubation with PD098059, a MAPK inhibitor, has no effect. Thus, T3-dependent tail regression does not require MAPKs, but a decrease in Cdk2 activity promotes tail regression.
机译：甲状腺激素（TH）3,5,3'-三碘甲甲状腺氨酸（T3 ）是多种细胞过程的重要调节剂，包括细胞增殖，分化和凋亡，越来越多的证据表明磷酸化蛋白质组的调节是TH介导的反应的重要因素。然而，关于磷酸化可能在发育过程中有助于T3 介导的细胞结果的机制了解甚少。细胞周期蛋白依赖性激酶（Cdks）和有丝分裂原激活的蛋白激酶（MAPK / ERK）已与哺乳动物细胞的TH信号传导有关。在这项研究中，我们研究了在青蛙中这些激酶可能在促进t变态过程中促进尾巴消退中的可能作用，meta是整个TH依赖的重要胚胎后过程。尾部Cdk2稳态水平和活性增加，并伴随着整个变态阶段的发展，随后急剧下降，这与尾部退化相吻合。细胞周期蛋白A相关的激酶活性也遵循类似的趋势，除了其相关的激酶活性在活性降低之前保持更长的时间。 ERK1和ERK2的蛋白质稳态水平保持相对恒定，并且它们的激酶活性直到尾巴回归期间才下降很多。在存在T3 的无血清培养基中培养的尾尖会发生退化，这与特定的Cdk2抑制剂共同孵育会加速。与M098抑制剂PD098059共同孵育无效。因此，依赖T3 的尾巴消退不需要MAPK，但是Cdk2活性的降低会促进尾巴消退。

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