中文摘要：为确保成功的长期侵染循环，菜豆金色花叶病毒必须控制其对寄主细胞的破坏作用，以预防植物可能出现激烈反应（至少在侵染初期时）。易感番茄植株会因粉虱介导感染病毒，而在其衰老前，单组分菜豆金色花叶病毒TYLCV并不会引起这些植株的过敏反应和细胞凋亡。至今，对于菜豆金色花叶病毒逃避植物抗性以及干扰细胞凋亡路径的方式仍知之甚少。本研究结果表明，分子伴侣HSP90（热休克蛋白90）及其辅助伴侣SGT1与TYLCV侵染有关。随着植物胁迫反应受抑制，TYLCV可在宽松的环境中复制与积累。
外文摘要：To ensure a successful long-term infection cycle, begomoviruses must restrain their destructive effect on host cells and prevent drastic plant responses, at least in the early stages of infection. The monopartite begomovirus Tomato yellow leaf curl virus (TYLCV) does not induce a hypersensitive response and cell death on whitefly-mediated infection of virus-susceptible tomato plants until diseased tomatoes become senescent. The way in which begomoviruses evade plant defences and interfere with cell death pathways is still poorly understood. We show that the chaperone HSP90 (heat shock protein 90) and its co-chaperone SGT1 (suppressor of the G2 allele of Skp1) are involved in the establishment of TYLCV infection. Inactivation of HSP90, as well as silencing of the Hsp90 and Sgt1 genes, leads to the accumulation of damaged ubiquitinated proteins and to a cell death phenotype. These effects are relieved under TYLCV infection. HSP90-dependent inactivation of 26S proteasome degradation and the transcriptional activation of the heat shock transcription factors HsfA2 and HsfB1 and of the downstream genes Hsp17 and Apx1/2 are suppressed in TYLCV-infected tomatoes. Following suppression of the plant stress response, TYLCV can replicate and accumulate in a permissive environment.
外文关键词：cell death；geminivirus；heat stress transcription factor；HSP90
作者：Moshe, Adi；Gorovits, Rena；Liu, Yule；等
作者单位：以色列希伯莱大学
期刊名称：MOLECULAR PLANT PATHOLOGY
期刊影响因子：4.335
出版年份：2016
出版刊次：2
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