The NPR1 ortholog PhaNPR1 is required for the induction of PhaPR1 in Phalaenopsis aphrodite.
The NPR1 ortholog PhaNPR1 is required for the induction of PhaPR1 in Phalaenopsis aphrodite.
复制标题
DOI：
10.1186/1999-3110-54-31
复制
发表时间：
2013-12
影响因子：
3.4
通讯作者：
Yeh HH
中科院分区：
文献类型：
--
作者：
Chen JC;Lu HC;Chen CE;Hsu HF;Chen HH;Yeh HH
系统获得性抗性（SAR）是一种有效的广谱防御机制，通过防御相关的水杨酸（SA）信号传导提供针对生物营养病原体的持久保护。在双子叶植物中，与SAR相关的基因已被广泛研究;然而，在单子叶植物中，在很大程度上仍未解决。NPR 1是一个进化保守的基因，在SAR中起着核心作用，PR-1被广泛用作有效SA信号传导的标记。我们确定了NPR 1和PR-1同源基因，PhaNPR 1和PhaPR 1，从一个经济上重要的兰花，蝴蝶兰aphrodite，并表征其在SA信号和建兰花叶病毒（CymMV）抗性的作用。NPR 1同源物的系统发育分析表明，这些基因似乎已经进化被子植物之前。与拟南芥NPR 1相似，PhaNPR 1在SA处理和CymMV感染后仅中度诱导。虽然PhaPR 1与AtPR 1的同源性仅为36%，但其启动子与其他PR-1基因的启动子具有相同的保守元件，并且在SA处理和CymMV感染后被诱导。在CymMV感染后，PhaNPR 1上的沉默也降低了PhaPR 1的表达;然而，CymMV积累不受影响。综上所述，病毒感染后，PhaNPR 1是诱导PhaPR 1所必需的，但在防御CymMV中几乎没有作用。本文的在线版本（doi：10.1186/1999-3110-54-31）包含补充材料，可供授权用户使用。
Systematic acquired resistance (SAR) is an effective broad-spectrum defense mechanism that confers long-lasting protection against biotrophic pathogens trough defense related salicylic acid (SA) signaling. Gene(s) involved in SAR have been extensively studied in dicot plants; however, remains largely unresolved in monocot plants. NPR1, an evolutionary conserved gene, plays a central role in SAR, and PR-1 is widely used as a marker for effective SA signaling. We identified NPR1 and PR-1 homologous genes, PhaNPR1 and PhaPR1, from an economically important orchid, Phalaenopsis aphrodite, and characterized their roles in SA signaling and Cymbidium mosaic virus (CymMV) resistance. A phylogenetic analysis of NPR1 homologs showed that these genes appear to have evolved before angiospermy. Similar to Arabidopsis NPR1, PhaNPR1 was only moderately induced upon SA treatment and CymMV infection. Although PhaPR1 shows only 36% identity with AtPR1, its promoter shared conserved elements with those of other PR-1 genes, and it was induced upon SA treatment and CymMV infection. After CymMV infection, silencing on PhaNPR1 also reduced PhaPR1 expression; however, CymMV accumulation was not affected. In conclusion, after virus infection, PhaNPR1 is required for PhaPR1 induction, but plays little role in defense against CymMV. The online version of this article (doi:10.1186/1999-3110-54-31) contains supplementary material, which is available to authorized users.