PDF(Pubmed)
Abstract：
CONCLUSIONS: The small-molecule glucosyltransferase loss-of-function mutant ugt76b1 exhibits both SID2- or NPR1-dependent and independent facets of enhanced plant immunity, whereupon FMO1 is required for the SID2 and NPR1 independence. The small-molecule glucosyltransferase UGT76B1 inactivates salicylic acid (SA), isoleucic acid (ILA), and N-hydroxypipecolic acid (NHP). ugt76b1 loss-of-function plants manifest an enhanced defense status. Thus, we were interested how UGT76B1 genetically integrates in defense pathways and whether all impacts depend on SA and NHP. We study the integration of UGT76B1 by transcriptome analyses of ugt76b1. The comparison of transcripts altered by the loss of UGT76B1 with public transcriptome data reveals both SA-responsive, ISOCHORISMATE SYNTHASE 1/SALICYLIC ACID INDUCTION DEFICIENT 2 (ICS1/SID2)- and NON EXPRESSOR OF PR GENES 1 (NPR1)-dependent, consistent with the role of UGT76B1 in glucosylating SA, and SA-non-responsive, SID2/NPR1-independent genes. We also discovered that UGT76B1 impacts on a group of genes showing non-SA-responsiveness and regulation by infections independent from SID2/NPR1. Enhanced resistance of ugt76b1 against Pseudomonas syringae is partially independent from SID2 and NPR1. In contrast, the ugt76b1-activated resistance is completely dependent on FMO1 encoding the NHP-synthesizing FLAVIN-DEPENDENT MONOOXYGENASE 1). Moreover, FMO1 ranks top among the ugt76b1-induced SID2- and NPR1-independent pathogen responsive genes, suggesting that FMO1 determines the SID2- and NPR1-independent effect of ugt76b1. Furthermore, the genetic study revealed that FMO1, ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1), SID2, and NPR1 are required for the SA-JA crosstalk and senescence development of ugt76b1, indicating that EDS1 and FMO1 have a similar effect like stress-induced SA biosynthesis (SID2) or the key SA signaling regulator NPR1. Thus, UGT76B1 influences both SID2/NPR1-dependent and independent plant immunity, and the SID2/NPR1 independence is relying on FMO1 and its product NHP, another substrate of UGT76B1.
摘要：
结论：小分子葡萄糖基转移酶功能丧失突变体ugt76b1表现出SID2-或NPR1依赖性和独立的植物免疫力增强方面，因此，SID2和NPR1独立需要FMO1。小分子葡萄糖基转移酶UGT76B1使水杨酸（SA）失活，异亮氨酸(ILA),和N-羟基羧酸(NHP)。ugt76b1丧失功能的植物表现出增强的防御状态。因此，我们感兴趣的是UGT76B1基因如何整合到防御途径中,以及是否所有影响都取决于SA和NHP.我们通过ugt76b1的转录组分析研究UGT76B1的整合。通过UGT76B1丢失而改变的转录本与公共转录组数据的比较揭示了两种SA反应，同工酶合成酶1/水杨酸诱导缺失2（ICS1/SID2）-和PR基因1（NPR1）依赖性的非表达，与UGT76B1在糖基化SA中的作用一致，和SA-无响应，SID2/NPR1独立基因。我们还发现UGT76B1对一组显示非SA反应性和独立于SID2/NPR1的感染调节的基因产生影响。ugt76b1对丁香假单胞菌的抗性增强部分独立于SID2和NPR1。相比之下,ugt76b1激活的电阻完全取决于FMO1编码NHP合成的黄素依赖性单氧酶1）。此外，FMO1在ugt76b1诱导的SID2-和NPR1-非依赖性病原体应答基因中排名第一，表明FMO1决定了ugt76b1的SID2-和NPR1-非依赖性效应。此外，遗传学研究表明，FMO1，增强疾病易感性1（EDS1），SA-JA串扰和ugt76b1的衰老发展需要SID2和NPR1，这表明EDS1和FMO1具有类似的作用，例如应激诱导的SA生物合成（SID2）或关键的SA信号传导调节剂NPR1。因此，UGT76B1影响SID2/NPR1依赖和独立的植物免疫，SID2/NPR1的独立性依赖于FMO1及其产品NHP，UGT76B1的另一种底物。
