文章快递：客户采用我司Amylose磁珠在高分期刊Cell Host & Microbe发表论文
2025-5-3 13:03:56点击：
Zhang X, Wang G, Zhang P, et al. Plant cell-cycle regulators control the nuclear environment for viral pathogenesis[J]. Cell Host & Microbe, 2025, 33(3): 420-435. e14.
Plant cell-cycle regulators control the nuclear environment for viral pathogenesis
植物细胞周期调节因子控制病毒发病机制的核环境
Highlights• Cell division cycle 20 secures RETINOBLASTOMA-RELATED 1 with E2F transcription factor
• 细胞分裂周期 20 用 E2F 转录因子确保视网膜母细胞瘤相关 1
• CDC20-coupled anaphase-promoting complex/cyclosome depletes cyclin D1
• CDC20 偶联的后期促进复合物/周期体消耗细胞周期蛋白 D1
• Viral pathogen hijacks APC/CCDC20 to disassociate RBR1-E2F complexes
• 病毒病原体劫持 APC/CCDC20 以解离 RBR1-E2F 复合物
•Viral pathogen occupies APC/CCDC20 to boost cyclin-D1-mediated RBR1 depletion
• 病毒病原体占据 APC/CCDC20 以促进细胞周期蛋白 D1 介导的 RBR1 耗竭
Summary
The proper regulation of cell-cycle regulators is curial for both viral replication and host-plant adaptive growth during the viral pathogenesis. Mechanisms on reorchestrating RETINOBLASTOMA-RELATED 1 (RBR1), repressor of E2F transcription factor, and downstream genes in host-virus interactions are unclear. Here, we discover that anaphase-promoting complex/cyclosome (APC/C) E3 ligase activator cell division cycle 20 (CDC20) in tomato binds RBR1 or mediates cyclin D1 depletion to preserve RBR1-E2F complexes, while geminivirus or crinivirus repurposes APC/CCDC20 activities to liberate E2Fs in two ways: activating APC/CCDC20 to deplete RBR1 or blocking APC/CCDC20 to stimulate cyclin-D1-mediated RBR1 depletion. The liberated E2Fs activate DNA polymerase or heat shock protein 70 gene transcription to favor virus propagation. The improper disruption of RBR1-E2F complexes via hijacking APC/CCDC20 causes the host growth repression. We uncover a scenario in which the virus co-opts host APC/CCDC20 to reprogram RBR1-E2F complex to favor its propagation while dampening host vitality.
细胞周期调节因子的适当调节对于病毒发病机制中的病毒复制和宿主植物适应性生长都是有效的。在宿主-病毒相互作用中重排视网膜母细胞瘤相关 1 （RBR1）、E2F 转录因子阻遏因子和下游基因的机制尚不清楚。在这里，我们发现番茄中的后期促进复合物/循环体 （APC/C） E3 连接酶激活剂细胞分裂周期 20 （CDC20） 结合 RBR1 或介导细胞周期蛋白 D1 耗竭以保留 RBR1-E2F 复合物，而双子病毒或甲壳病毒重新利用 APC/CCDC20 活性以两种方式释放 E2F：激活 APC/CCDC20 以消耗 RBR1 或阻断 APC/CCDC20刺激细胞周期蛋白 D1 介导的 RBR1 耗竭。释放的 E2F 激活 DNA 聚合酶或热休克蛋白 70 基因转录，有利于病毒繁殖。通过劫持 APC/CCDC20 对 RBR1-E2F 复合物的不当破坏会导致宿主生长抑制。我们揭示了一种情况，其中病毒选择宿主 APC/CCDC20 重新编程 RBR1-E2F 复合物以促进其传播，同时抑制宿主活力。
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Graphical abstract
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