Zhang Kai, Lu Huixiang, Wan Chuanfang, Tang Daobin, Zhao Yong, Luo Kai, Li Shixi, Wang Jichun
College of Agronomy and Biotechnology, Southwest University, Beibei, Chongqing 400715, China.
Key Laboratory of Biology and Genetic Breeding for Tuber and Root Crops in Chongqing, Beibei, Chongqing 400715, China.
Plants (Basel). 2020 Apr 10;9(4):492. doi: 10.3390/plants9040492.
Sweet potato virus disease (SPVD) is the most devastating viral disease in sweet potato ( (L.) Lam.), causing substantial yield losses worldwide. We conducted a systemic investigation on the spread, transmission, and pathogenesis of SPVD. Field experiments conducted over two years on ten sweet potato varieties showed that SPVD symptoms first occurred in newly developed top leaves, and spread from adjacent to distant plants in the field. The SPVD incidence was mainly (but not only) determined by the resistance of the varieties planted, and each variety exhibited a characteristic subset of SPVD symptoms. SPVD was not robustly transmitted through friction inoculation, but friction of the main stem might contribute to a higher SPVD incidence rate compared to friction of the leaf and branch tissues. Furthermore, our results suggested that SPVD might be latent in the storage root. Therefore, using virus-free storage roots and cuttings, purposeful monitoring for SPVD according to variety-specific symptoms, and swiftly removing infected plants (especially during the later growth stages) would help control and prevent SPVD during sweet potato production. Comparative transcriptome analysis revealed that numerous genes involved in photosynthesis, starch and sucrose metabolism, flavonoid biosynthesis, and carotenoid biosynthesis were downregulated following SPVD, whereas those involved in monolignol biosynthesis, zeatin biosynthesis, trehalose metabolism, and linoleic acid metabolism were upregulated. Notably, critical genes involved in pathogenesis and plant defense were significantly induced or suppressed following SPVD. These data provide insights into the molecular changes of sweet potato in response to SPVD and elucidate potential SPVD pathogenesis and defense mechanisms in sweet potato. Our study provides important information that can be used to tailor sustainable SPVD control strategies and guide the molecular breeding of SPVD-resistant sweet potato varieties.
甘薯病毒病(SPVD)是甘薯(Ipomoea batatas (L.) Lam.)中最具毁灭性的病毒病,在全球范围内造成了巨大的产量损失。我们对SPVD的传播、传播途径和发病机制进行了系统研究。在两年时间里对十个甘薯品种进行的田间试验表明,SPVD症状首先出现在新长出的顶部叶片上,并在田间从相邻植株传播到远处植株。SPVD的发病率主要(但不限于)由所种植品种的抗性决定,每个品种都表现出特定的SPVD症状子集。SPVD不能通过摩擦接种有效传播,但与叶片和枝条组织的摩擦相比,主茎的摩擦可能导致更高的SPVD发病率。此外,我们的结果表明SPVD可能潜伏在贮藏根中。因此,使用无病毒的贮藏根和插条,根据品种特异性症状有针对性地监测SPVD,并迅速清除受感染植株(尤其是在生长后期),将有助于在甘薯生产过程中控制和预防SPVD。比较转录组分析显示,SPVD后,许多参与光合作用、淀粉和蔗糖代谢、类黄酮生物合成和类胡萝卜素生物合成的基因表达下调,而参与木质素单体生物合成、玉米素生物合成、海藻糖代谢和亚油酸代谢的基因表达上调。值得注意的是,参与发病机制和植物防御的关键基因在SPVD后显著诱导或抑制。这些数据提供了甘薯对SPVD响应的分子变化见解,阐明了甘薯潜在的SPVD发病机制和防御机制。我们的研究提供了重要信息,可用于制定可持续的SPVD控制策略,并指导抗SPVD甘薯品种的分子育种。