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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >A viral adaptor protein modulating casein kinase II activity induces cytopathic effects in permissive cells
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A viral adaptor protein modulating casein kinase II activity induces cytopathic effects in permissive cells

机译：调节酪蛋白激酶II活性的病毒衔接蛋白诱导宽容细胞的细胞病变作用

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摘要

Autonomous parvoviruses induce severe morphological and physiological alterations in permissive host cells, eventually leading to cell lysis and release of progeny virions. Viral cytopathic effects (CPE) result from specific rearrangements and destruction of cy-toskeletal micro- and intermediate filaments. We recently reported that inhibition of endogenous casein kinase II (CKII) protects target cells from parvovirus minute virus of mice (MVM)-induced CPE, pointing to this kinase as an effector of MVM toxicity. The present work shows that the parvoviral NS1 protein mediates CKII-depen-dent cytoskeletal alterations and cell death. NS1 can act as an adaptor molecule, linking the cellular protein kinase CKIIα to tropomyosin and thus modulating the substrate specificity of the kinase. This action results in an altered tropomyosin phosphory-lation pattern both in vitro and in living cells. The capacity of NS1 to induce CPE was impaired by mutations abolishing binding with either CKIIα or tropomyosin. The cytotoxic adaptor function of NS1 was confirmed with fusion peptides, where the tropomyosin-binding domain of NS1 and CKIIα are physically linked. These adaptor peptides were able to mimic NS1 in its ability to induce death of transformed MVM-permissive cells.
机译：自主细小病毒在允许的宿主细胞中诱导严重的形态和生理变化，最终导致细胞裂解和后代病毒体释放。病毒细胞病变效应（CPE）是由细胞骨架微细丝和中间细丝的特定重排和破坏引起的。我们最近报道，内源性酪蛋白激酶II（CKII）的抑制保护目标细胞免受小鼠细小病毒微小病毒（MVM）诱导的CPE的侵害，并指出该激酶是MVM毒性的效应子。目前的工作表明，细小病毒NS1蛋白介导CKII依赖的细胞骨架改变和细胞死亡。 NS1可以充当衔接子分子，将细胞蛋白激酶CKIIα连接到原肌球蛋白，从而调节激酶的底物特异性。该作用导致体外和活细胞中原肌球蛋白磷酸化模式的改变。取消与CKIIα或原肌球蛋白结合的突变会削弱NS1诱导CPE的能力。用融合肽证实了NS1的细胞毒性衔接子功能，其中NS1的原肌球蛋白结合结构域与CKIIα物理连接。这些衔接子肽能够模拟NS1诱导转化的MVM允许细胞死亡的能力。

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