文章快遞：客戶采用我司Amylose磁珠在高分期刊Cell Host & Microbe發(fā)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(diào)節(jié)因子控制病毒發(fā)病機制的核環(huán)境
Highlights? Cell division cycle 20 secures RETINOBLASTOMA-RELATED 1 with E2F transcription factor
? 細胞分裂周期 20 用 E2F 轉(zhuǎn)錄因子確保視網(wǎng)膜母細胞瘤相關(guān) 1
? CDC20-coupled anaphase-promoting complex/cyclosome depletes cyclin D1
? CDC20 偶聯(lián)的后期促進復(fù)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(fù)合物
?Viral pathogen occupies APC/CCDC20 to boost cyclin-D1-mediated RBR1 depletion
? 病毒病原體占據(jù) APC/CCDC20 以促進細胞周期蛋白 D1 介導(dǎo)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(diào)節(jié)因子的適當(dāng)調(diào)節(jié)對于病毒發(fā)病機制中的病毒復(fù)制和宿主植物適應(yīng)性生長都是有效的。在宿主-病毒相互作用中重排視網(wǎng)膜母細胞瘤相關(guān) 1 （RBR1）、E2F 轉(zhuǎn)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(fā)現(xiàn)番茄中的后期促進復(fù)合物/循環(huán)體 （APC/C） E3 連接酶激活劑細胞分裂周期 20 （CDC20） 結(jié)合 RBR1 或介導(dǎo)細胞周期蛋白 D1 耗竭以保留 RBR1-E2F 復(fù)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(dǎo)的 RBR1 耗竭。釋放的 E2F 激活 DNA 聚合酶或熱休克蛋白 70 基因轉(zhuǎn)錄，有利于病毒繁殖。通過劫持 APC/CCDC20 對 RBR1-E2F 復(fù)合物的不當(dāng)破壞會導(dǎo)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(fù)合物以促進其傳播，同時抑制宿主活力。
客戶在論文中采用我司的Si-Amylose磁珠釣取MBP標簽蛋白，更多磁珠信息請參考 http://m.5000js.com/Product/1354985925.html
Graphical abstract
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