文章快遞：客戶采用我司Amylose磁珠在高分期刊Cell Host & Microbe發表論文
2025-5-3 13:03:56點擊：
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
植物細胞周期調節因子控制病毒發病機制的核環境
Highlights? Cell division cycle 20 secures RETINOBLASTOMA-RELATED 1 with E2F transcription factor
? 細胞分裂周期 20 用 E2F 轉錄因子確保視網膜母細胞瘤相關 1
? CDC20-coupled anaphase-promoting complex/cyclosome depletes cyclin D1
? CDC20 偶聯的后期促進復合物/周期體消耗細胞周期蛋白 D1
? Viral pathogen hijacks APC/CCDC20 to disassociate RBR1-E2F complexes
? 病毒病原體劫持 APC/CCDC20 以解離 RBR1-E2F 復合物
?Viral pathogen occupies APC/CCDC20 to boost cyclin-D1-mediated RBR1 depletion
? 病毒病原體占據 APC/CCDC20 以促進細胞周期蛋白 D1 介導的 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.
細胞周期調節因子的適當調節對于病毒發病機制中的病毒復制和宿主植物適應性生長都是有效的。在宿主-病毒相互作用中重排視網膜母細胞瘤相關 1 （RBR1）、E2F 轉錄因子阻遏因子和下游基因的機制尚不清楚。在這里，我們發現番茄中的后期促進復合物/循環體 （APC/C） E3 連接酶激活劑細胞分裂周期 20 （CDC20） 結合 RBR1 或介導細胞周期蛋白 D1 耗竭以保留 RBR1-E2F 復合物，而雙子病毒或甲殼病毒重新利用 APC/CCDC20 活性以兩種方式釋放 E2F：激活 APC/CCDC20 以消耗 RBR1 或阻斷 APC/CCDC20刺激細胞周期蛋白 D1 介導的 RBR1 耗竭。釋放的 E2F 激活 DNA 聚合酶或熱休克蛋白 70 基因轉錄，有利于病毒繁殖。通過劫持 APC/CCDC20 對 RBR1-E2F 復合物的不當破壞會導致宿主生長抑制。我們揭示了一種情況，其中病毒選擇宿主 APC/CCDC20 重新編程 RBR1-E2F 復合物以促進其傳播，同時抑制宿主活力。
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Graphical abstract
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