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首页> 外文期刊>Molecular and Cellular Biology >Regulation of microtubule dynamics by Ca2+/calmodulin-dependent kinase IV/Gr-dependent phosphorylation of oncoprotein 18.
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Regulation of microtubule dynamics by Ca2+/calmodulin-dependent kinase IV/Gr-dependent phosphorylation of oncoprotein 18.

机译：Ca2 + /钙调蛋白依赖性激酶IV / Gr依赖性癌蛋白18磷酸化对微管动力学的调节。

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Oncoprotein 18 (Op18; also termed p19, 19K, p18, prosolin, and stathmin) is a regulator of microtubule (MT) dynamics and is phosphorylated by multiple kinase systems on four Ser residues. In addition to cell cycle-regulated phosphorylation, external signals induce phosphorylation of Op18 on Ser-25 by the mitogen-activated protein kinase and on Ser-16 by the Ca2+/calmodulin-dependent kinase IV/Gr (CaMK IV/Gr). Here we show that induced expression of a constitutively active mutant of CaMK IV/Gr results in phosphorylation of Op18 on Ser-16. In parallel, we also observed partial degradation of Op18 and a rapid increase of total cellular MTs. These results suggest a link between CaMK IV/Gr, Op18, and MT dynamics. To explore such a putative link, we optimized a genetic system that allowed conditional coexpression of a series of CaMK IV/Gr and Op18 derivatives. The result shows that CaMK IV/Gr can suppress the MT-regulating activity of Op18 by phosphorylation on Ser-16. In line with these results, by employing a chemical cross-linking protocol, it was shown that phosphorylation of Ser-16 is involved in weakening of the interactions between Op18 and tubulin. Taken together, these data suggest that the mechanism of CaMK IV/Gr-mediated suppression of Op18 activity involves both partial degradation of Op18 and direct modulation of the MT-destabilizing activity of this protein. These results show that Op18 phosphorylation by CaMK IV/Gr may couple alterations of MT dynamics in response to external signals that involve Ca2+.
机译：癌蛋白18（Op18;也称为p19、19K，p18，prosolin和stathmin）是微管（MT）动力学的调节剂，并由多个激酶系统在四个Ser残基上磷酸化。除了细胞周期调节的磷酸化外，外部信号还通过丝裂原激活的蛋白激酶诱导Ser-25上的Op18磷酸化，并通过Ca2 + /钙调蛋白依赖性激酶IV / Gr（CaMK IV / Gr）诱导Ser-16上的Op18磷酸化。在这里，我们表明，CaMK IV / Gr组成型活性突变体的诱导表达导致Ser-16上的Op18磷酸化。同时，我们还观察到Op18的部分降解和总细胞MT的快速增加。这些结果表明CaMK IV / Gr，Op18和MT动力学之间存在联系。为了探索这种假定的联系，我们优化了一个遗传系统，该遗传系统允许一系列CaMK IV / Gr和Op18衍生物的条件共表达。结果表明，CaMK IV / Gr通过在Ser-16上磷酸化可以抑制Op18的MT调节活性。与这些结果一致，通过采用化学交联方案，表明Ser-16的磷酸化与Op18和微管蛋白之间的相互作用的减弱有关。综上所述，这些数据表明CaMK IV / Gr介导的Op18活性抑制机制涉及Op18的部分降解和该蛋白MT失稳活性的直接调节。这些结果表明，由CaMK IV / Gr引起的Op18磷酸化可偶联MT动力学的变化，以响应涉及Ca2 +的外部信号。

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