Tomato yellow leaf curl virus infection mitigates the heat stress response of plants grown at high temperatures.
Tomato yellow leaf curl virus infection mitigates the heat stress response of plants grown at high temperatures.
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DOI：
10.1038/srep19715
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发表时间：
2016-01-21
影响因子：
4.6
通讯作者：
Gorovits R
中科院分区：
文献类型：
--
作者：
Anfoka G;Moshe A;Fridman L;Amrani L;Rotem O;Kolot M;Zeidan M;Czosnek H;Gorovits R
培养的番茄经常暴露在极端高温和番茄黄曲叶病毒（TYLCV）感染的环境中。这种胁迫组合会导致严重的疾病症状和产量损失。比较了 TYLCV 敏感和抗性番茄对热应激和病毒感染的反应。 TYLCV 感染植物的热应激反应受到破坏。这种下降与热休克转录因子 (HSF) HSFA2 和 HSFB1 的下调相关，从而与 HSF 调节基因 Hsp17、Apx1、Apx2 和 Hsp90 的下调相关。我们认为热应激反应减弱是由于 HSFA2 易位到受感染细胞核的能力下降所致。所有6种TYLCV蛋白均能够在体外与番茄HSFA2相互作用，而且外壳蛋白在细胞核中与HSFA2形成复合物。病毒蛋白捕获 HSFA2 可以抑制热应激反应基因的转录激活。热应激和 TYLCV 应激的应用伴随着含有 TYLCV 蛋白和 DNA 的细胞内大蛋白聚集体的形成。即使在从热应激中恢复后，细胞伴侣仍保持聚集状态，这会阻止游离可溶性伴侣的循环，导致应激反应效率进一步降低。
Cultured tomatoes are often exposed to a combination of extreme heat and infection with Tomato yellow leaf curl virus (TYLCV). This stress combination leads to intense disease symptoms and yield losses. The response of TYLCV-susceptible and resistant tomatoes to heat stress together with viral infection was compared. The plant heat-stress response was undermined in TYLCV infected plants. The decline correlated with the down-regulation of heat shock transcription factors (HSFs) HSFA2 and HSFB1, and consequently, of HSF-regulated genes Hsp17, Apx1, Apx2 and Hsp90. We proposed that the weakened heat stress response was due to the decreased capacity of HSFA2 to translocate into the nuclei of infected cells. All the six TYLCV proteins were able to interact with tomato HSFA2 in vitro, moreover, coat protein developed complexes with HSFA2 in nuclei. Capturing of HSFA2 by viral proteins could suppress the transcriptional activation of heat stress response genes. Application of both heat and TYLCV stresses was accompanied by the development of intracellular large protein aggregates containing TYLCV proteins and DNA. The maintenance of cellular chaperones in the aggregated state, even after recovery from heat stress, prevents the circulation of free soluble chaperones, causing an additional decrease in stress response efficiency.