Rotavirus infection induces G1 to S phase transition in MA104 cells via Ca⁺²/Calmodulin pathway.
Rotavirus infection induces G1 to S phase transition in MA104 cells via Ca⁺²/Calmodulin pathway.
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DOI：
10.1016/j.virol.2014.03.001
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发表时间：
2014-04
期刊：
影响因子：
3.7
通讯作者：
Chawla-Sarkar M
中科院分区：
文献类型：
--
作者：
Bhowmick R;Banik G;Chanda S;Chattopadhyay S;Chawla-Sarkar M
病毒，专性细胞寄生虫依赖于宿主细胞功能，并靶向宿主细胞周期以获得自身利益。本研究探讨轮状病毒感染对细胞周期的影响。我们发现轮状病毒（RV）感染MA 104细胞可诱导细胞周期蛋白和细胞周期蛋白依赖性激酶的表达，并下调CDK抑制剂的表达，导致细胞发生G1期向S期的转变。发现轮状病毒诱导的S期积累与钙调蛋白表达的诱导和CaMKI的激活同时发生，CaMKI被报道为G1-S相变的诱导剂。发现这种细胞周期操纵是Ca+2/钙调素途径依赖的。当发现轮状病毒感染期间，与非同步化细胞相比，在S期同步化细胞中病毒基因表达以及病毒滴度增加，而在G 0/G1期同步化细胞中病毒基因表达以及病毒滴度降低时，建立了G1至S期转变的生理相关性。轮状病毒感染诱导细胞聚集在细胞周期的S期。S期细胞的这种积累是Ca+2/CaM信号通路依赖的。S期细胞的积累有助于病毒的生长。
Viruses, obligate cellular parasites rely on host cellular functions and target the host cell cycle for their own benefit. In this study, effect of rotavirus infection on cell cycle machinery was explored. We found that rotavirus (RV) infection in MA104 cells induces the expression of cyclins and cyclin dependent kinases and down-regulates expression of CDK inhibitors, resulting in G1 to S phase transition. The rotavirus induced S phase accumulation was found to be concurrent with induction in expression of calmodulin and activation of CaMKI which is reported as inducer of G1–S phase transition. This cell cycle manipulation was found to be Ca+2/Calmodulin pathway dependent. The physiological relevance of G1 to S phase transition was established when viral gene expressions as well as viral titers were found to be increased in S phase synchronized cells and decreased in G0/G1 phase synchronized cells compared to unsynchronized cells during rotavirus infection. Rotavirus infection induces cells to accumulate in S phase of cell cycle. This accumulation of cells in S phase is Ca+2/CaM signaling pathway dependent. Accumulation of cells in S phase helps in viral growth.
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