Núcleo de Biotecnologia, Universidade Federal do Espírito Santo, Av. Marechal Campos, 1468, Vitória, ES, 29040-090, Brazil.
Núcleo Multidisciplinar de Pesquisa-Polo de Xerém, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brazil.
Plant Cell Rep. 2018 Jul;37(7):967-980. doi: 10.1007/s00299-018-2281-x. Epub 2018 Mar 21.
Global gene expression analysis indicates host stress responses, mainly those mediated by SA, associated to the tolerance to sticky disease symptoms at pre-flowering stage in Carica papaya. Carica papaya plants develop the papaya sticky disease (PSD) as a result of the combined infection of papaya meleira virus (PMeV) and papaya meleira virus 2 (PMeV2), or PMeV complex. PSD symptoms appear only after C. papaya flowers. To understand the mechanisms involved in this phenomenon, the global gene expression patterns of PMeV complex-infected C. papaya at pre-and post-flowering stages were assessed by RNA-Seq. The result was 633 and 88 differentially expressed genes at pre- and post-flowering stages, respectively. At pre-flowering stage, genes related to stress and transport were up-regulated while metabolism-related genes were down-regulated. It was observed that induction of several salicylic acid (SA)-activated genes, including PR1, PR2, PR5, WRKY transcription factors, ROS and callose genes, suggesting SA signaling involvement in the delayed symptoms. In fact, pre-flowering C. papaya treated with exogenous SA showed a tendency to decrease the PMeV and PMeV2 loads when compared to control plants. However, pre-flowering C. papaya also accumulated transcripts encoding a NPR1-inhibitor (NPR1-I/NIM1-I) candidate, genes coding for UDP-glucosyltransferases (UGTs) and several genes involved with ethylene pathway, known to be negative regulators of SA signaling. At post-flowering, when PSD symptoms appeared, the down-regulation of PR-1 encoding gene and the induction of BSMT1 and JA metabolism-related genes were observed. Hence, SA signaling likely operates at the pre-flowering stage of PMeV complex-infected C. papaya inhibiting the development of PSD symptoms, but the induction of its negative regulators prevents the full-scale and long-lasting tolerance.
全球基因表达分析表明，与开花前阶段对粘性疾病症状的耐受性相关的宿主应激反应主要是由水杨酸（SA）介导的。番木瓜受番木瓜环斑病毒（PMeV）和番木瓜环斑病毒 2（PMeV2）或 PMeV 复合感染会发展为番木瓜粘性病（PSD）。PSD 症状仅在番木瓜开花后出现。为了了解这种现象涉及的机制，通过 RNA-Seq 评估了 PMeV 复合感染番木瓜在开花前和开花后的全基因表达模式。结果分别在开花前和开花后阶段鉴定到 633 个和 88 个差异表达基因。在开花前阶段，与应激和运输相关的基因上调，而与代谢相关的基因下调。观察到几种水杨酸（SA）激活基因的诱导，包括 PR1、PR2、PR5、WRKY 转录因子、ROS 和胼胝质基因，表明 SA 信号参与了症状的延迟。事实上，与对照植物相比，外源 SA 处理的开花前番木瓜表现出降低 PMeV 和 PMeV2 负荷的趋势。然而，开花前番木瓜也积累了编码 NPR1 抑制剂（NPR1-I/NIM1-I）候选物、编码 UDP-葡萄糖基转移酶（UGTs）和几个与乙烯途径相关的基因的转录本，这些基因已知是 SA 信号的负调节剂。在开花后出现 PSD 症状时，观察到 PR-1 编码基因的下调以及 BSMT1 和 JA 代谢相关基因的诱导。因此，SA 信号可能在 PMeV 复合感染番木瓜的开花前阶段起作用，抑制 PSD 症状的发展，但对其负调节剂的诱导阻止了全面和持久的耐受性。
