Baebler Š, Witek K, Petek M, Stare K, Tušek-Žnidarič M, Pompe-Novak M, Renaut J, Szajko K, Strzelczyk-Żyta D, Marczewski W, Morgiewicz K, Gruden K, Hennig J
National Institute of Biology, Večna pot 111, 1000 Ljubljana, Slovenia.
J Exp Bot. 2014 Mar;65(4):1095-109. doi: 10.1093/jxb/ert447. Epub 2014 Jan 13.
The purpose of the study was to investigate the role of salicylic acid (SA) signalling in Ny-1-mediated hypersensitive resistance (HR) of potato (Solanum tuberosum L.) to Potato virus Y (PVY). The responses of the Ny-1 allele in the Rywal potato cultivar and transgenic NahG-Rywal potato plants that do not accumulate SA were characterized at the cytological, biochemical, transcriptome, and proteome levels. Analysis of noninoculated and inoculated leaves revealed that HR lesions started to develop from 3 d post inoculation and completely restricted the virus spread. At the cytological level, features of programmed cell death in combination with reactive oxygen species burst were observed. In response to PVY infection, SA was synthesized de novo. The lack of SA accumulation in the NahG plants led to the disease phenotype due to unrestricted viral spreading. Grafting experiments show that SA has a critical role in the inhibition of PVY spreading in parenchymal tissue, but not in vascular veins. The whole transcriptome analysis confirmed the central role of SA in orchestrating Ny-1-mediated responses and showed that the absence of SA leads to significant changes at the transcriptome level, including a delay in activation of expression of genes known to participate in defence responses. Moreover, perturbations in the expression of hormonal signalling genes were detected, shown as a switch from SA to jasmonic acid/ethylene signalling. Viral multiplication in the NahG plants was accompanied by downregulation of photosynthesis genes and activation of multiple energy-producing pathways.
本研究的目的是调查水杨酸(SA)信号在马铃薯(Solanum tuberosum L.)Ny-1介导的对马铃薯Y病毒(PVY)的过敏反应抗性(HR)中的作用。在细胞学、生化、转录组和蛋白质组水平上,对不积累SA的Rywal马铃薯品种和转基因NahG-Rywal马铃薯植株中Ny-1等位基因的反应进行了表征。对未接种和接种叶片的分析表明,HR损伤在接种后3天开始出现,并完全限制了病毒传播。在细胞学水平上,观察到程序性细胞死亡与活性氧爆发相结合的特征。响应PVY感染,SA从头合成。NahG植株中SA积累的缺乏由于病毒不受限制的传播而导致了病害表型。嫁接实验表明,SA在抑制PVY在薄壁组织中的传播中起关键作用,但在维管束中不起作用。全转录组分析证实了SA在协调Ny-1介导的反应中的核心作用,并表明SA的缺失导致转录组水平上的显著变化,包括参与防御反应的已知基因表达激活的延迟。此外,检测到激素信号基因表达的扰动,表现为从SA信号转换为茉莉酸/乙烯信号。NahG植株中的病毒增殖伴随着光合作用基因的下调和多种能量产生途径的激活。