Mechanism underlying potato spindle tuber viroid affecting tomato (Solanum lycopersicum): loss of control over reactive oxygen species production
Mechanism underlying potato spindle tuber viroid affecting tomato (Solanum lycopersicum): loss of control over reactive oxygen species production
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DOI：
10.1007/s10327-021-01000-1
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发表时间：
2021-03-25
影响因子：
1.2
通讯作者：
Sano, Teruo
中科院分区：
文献类型：
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作者：
Fujibayashi, Misato;Suzuki, Takahiro;Sano, Teruo
马铃薯纺锤块茎类病毒（PSTVd）变异体严重感染番茄栽培品种“Rutgers”导致系统发育迟缓、叶片畸形和脉坏死;伴随着活性氧（ROS）的快速增加和应激响应microRNA（miR 398和miR 398 a-3 p）的异常高表达。症状的严重程度、PSTVd的积累、miR 398和miR 398 a-3 p的高表达以及高水平的ROS产生与PSTVd变异体的发病正相关。相反，细胞质和叶绿体定位的Cu/Zn-超氧化物歧化酶基因SlSOD 4和SlSOD 3，分别编码的ROS清除酶下调，并与症状的严重程度呈负相关。相反，在PSTVd感染，PSTVd耐受（几乎无症状）番茄品种'Moneymaker'，其中PSTVd积累受到抑制，ROS的产生与对照一样低，miR 398和miR 398 a-3 p下调，几乎所有的SOD基因上调。结果表明，在PSTVd敏感的番茄品种'Rutgers'，感染严重的PSTVd变体引起抑制的细胞质和叶绿体定位的Cu/Zn-SOD基因通过PSTVd诱导的miR 398和miR 398 a-3的过表达，分别。这种情况显著降低或消除了正常的ROS清除功能，并且细胞和组织中过量的有害ROS似乎已经引起了伴随坏死的严重病理症状。
Severe infection of the tomato cultivar 'Rutgers' with potato spindle tuber viroid (PSTVd) variants resulted in systemic stunting, leaf malformation, and vein necrosis; accompanied by a rapid increase in reactive oxygen species (ROS) and abnormally high expression of the stress-responsive microRNAs, miR398 and miR398a-3p. The severity of the symptoms, PSTVd accumulation, the high expression of miR398 and miR398a-3p, and the high level of ROS production were positively correlated with the pathogenesis of the PSTVd variants. In contrast, the cytosolic and chloroplast-localized Cu/Zn-superoxide dismutase genes SlSOD4 and SlSOD3, respectively that encode the ROS scavenging enzymes were down-regulated and negatively correlated with the severity of the symptoms. Conversely, in the PSTVd-infected, PSTVd-tolerant (almost asymptomatic) tomato cultivar 'Moneymaker' in which PSTVd accumulation was suppressed, the ROS production was as low as in the control, miR398 and miR398a-3p were down-regulated, and almost all the SOD genes were up-regulated. The results indicated that in the PSTVd-sensitive tomato cultivar 'Rutgers', infection with the severe PSTVd variant caused suppression of the cytosolic and chloroplast-localized Cu/Zn-SOD genes via PSTVd-induced overexpression of miR398 and miR398a-3, respectively. This condition significantly reduced or eliminated the normal ROS scavenging function and an excess of harmful ROS in cells and tissues seem to have caused severe pathological symptoms accompanied by necrosis.