The trade-off between growth and defense is a critical aspect of plant immunity. Therefore, plant immune response needs to be tightly regulated. The hormone regulating plant defense against biotrophic pathogens is salicylic acid (SA). Recently, N-hydroxy-pipecolic acid (NHP) was identified as second regulator for plant innate immunity and systemic acquired resistance. Although the biosynthetic pathway leading to NHP formation has already been identified, the route how NHP is further metabolized was unclear. Here, we present UGT76B1 as a UDP-dependent glycosyltransferase that modifies NHP by catalyzing the formation of 1-O-glucosyl-pipecolic acid (NHP-OGlc). Analysis of T-DNA and CRISPR knock-out mutant lines of UGT76B1 by targeted and non-targeted UHPLC-HRMS underlined NHP and SA as endogenous substrates of this enzyme in response to Pseudomonas infection and UV treatment. UGT76B1 shows similar KM for NHP and SA. ugt76b1 mutant plants have a dwarf phenotype and a constitutive defense response which can be suppressed by loss of function of the NHP biosynthetic enzyme FMO1. This suggests that elevated accumulation of NHP contributes to the enhanced disease resistance in ugt76b1. Externally applied NHP can move to distal tissue in ugt76b1 mutant plants. Although glycosylation is not required for the long distance movement of NHP during systemic acquired resistance, it is crucial to balance growth and defense.

中文翻译：

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糖基转移酶UGT76B1对于植物免疫至关重要，因为它控制着N-羟基-哌酸的体内稳态

生长与防御之间的权衡是植物免疫力的关键方面。因此，需要严格调节植物的免疫反应。调节植物抵抗生物营养性病原体防御的激素是水杨酸（SA）。最近，N-羟基哌酸（NHP）被确定为植物固有免疫力和系统获得性抗性的第二调节剂。尽管已经确定了导致NHP形成的生物合成途径，但是如何进一步代谢NHP的途径尚不清楚。在这里，我们提出了UGT76B1作为UDP依赖的糖基转移酶，它通过催化1-O-葡萄糖基-哌酸（NHP-OGlc）的形成来修饰NHP。通过靶向和非靶向UHPLC-HRMS对UGT76B1的T-DNA和CRISPR敲除突变株进行分析，强调了NHP和SA作为该酶的内源底物，响应假单胞菌感染和紫外线处理。UGT76B1对于NHP和SA显示相似的KM。ugt76b1突变植物具有矮表型和本构防御反应，可以通过NHP生物合成酶FMO1的功能丧失来抑制。这表明NHP积累的增加有助于ugt76b1抗病性的增强。外部应用的NHP可以移动到ugt76b1突变植物的远端组织。尽管在系统性获得性抵抗期间NHP的长距离运动不需要糖基化，但平衡生长和防御至关重要。ugt76b1突变植物具有矮表型和本构防御反应，可以通过NHP生物合成酶FMO1的功能丧失来抑制。这表明NHP积累的增加有助于ugt76b1抗病性的增强。外部应用的NHP可以移动到ugt76b1突变植物的远端组织。尽管在系统性获得性抵抗期间NHP的长距离运动不需要糖基化，但平衡生长和防御至关重要。ugt76b1突变植物具有矮表型和本构防御反应，可以通过NHP生物合成酶FMO1的功能丧失来抑制。这表明NHP积累的增加有助于ugt76b1抗病性的增强。外部应用的NHP可以移动到ugt76b1突变植物的远端组织。尽管在系统性获得性抵抗期间NHP的长距离运动不需要糖基化，但平衡生长和防御至关重要。