Pseudomonas syringae type III effector HopAF1 suppresses plant immunity by targeting methionine recycling to block ethylene induction.
Pseudomonas syringae type III effector HopAF1 suppresses plant immunity by targeting methionine recycling to block ethylene induction.
复制标题
丁香假单胞菌 III 型效应子 HopAF1 通过靶向蛋氨酸回收来阻止乙烯诱导，从而抑制植物免疫。
DOI：
10.1073/pnas.1606322113
复制
发表时间：
2016
影响因子：
11.1
通讯作者：
Washington EJ
中科院分区：
文献类型：
--
作者：
Washington EJ
HopAF1是一种功能未知的III型效应蛋白，编码于几种丁香假单胞菌和其他植物病原体的基因组中。结构模型预测HopAF1与脱酰胺酶蛋白密切相关。脱酰胺是指酰胺基与羧酸基的不可逆取代。几种细菌毒力因子是操纵特定宿主蛋白底物活性的脱酰胺酶。我们发现拟南芥甲基硫代腺苷核苷酶蛋白MTN1和MTN2可能是HopAF1脱酰胺的靶点。mtn是阳循环中的酶，对拟南芥高水平的乙烯生物合成至关重要。我们假设HopAF1通过操纵MTN活性和乙烯水平来抑制宿主防御反应。我们确定细菌传递的HopAF1抑制由病原体相关分子模式诱导的乙烯生物合成，并且拟南芥mtn1 mtn2突变体植株表型上表现出HopAF1的作用。此外，我们在拟南芥的MTN1和MTN2中发现了两种保守的天冬酰胺，当通过位点特异性突变被脱酰胺时，它们会导致功能表型的丧失。这些残基是HopAF1脱酰胺的潜在靶点。HopAF1介导的Yang cycle MTN蛋白操纵可能是一种进化保守的机制，即来自多种植物病原体的HopAF1同源物在多种植物宿主中导致疾病。
HopAF1 is a type III effector protein of unknown function encoded in the genomes of several strains ofPseudomonas syringaeand other plant pathogens. Structural modeling predicted that HopAF1 is closely related to deamidase proteins. Deamidation is the irreversible substitution of an amide group with a carboxylate group. Several bacterial virulence factors are deamidases that manipulate the activity of specific host protein substrates. We identifiedArabidopsismethylthioadenosine nucleosidase proteins MTN1 and MTN2 as putative targets of HopAF1 deamidation. MTNs are enzymes in the Yang cycle, which is essential for the high levels of ethylene biosynthesis inArabidopsis. We hypothesized that HopAF1 inhibits the host defense response by manipulating MTN activity and consequently ethylene levels. We determined that bacterially delivered HopAF1 inhibits ethylene biosynthesis induced by pathogen-associated molecular patterns and thatArabidopsis mtn1 mtn2mutant plants phenocopy the effect of HopAF1. Furthermore, we identified two conserved asparagines in MTN1 and MTN2 fromArabidopsisthat confer loss of function phenotypes when deamidated via site-specific mutation. These residues are potential targets of HopAF1 deamidation. HopAF1-mediated manipulation of Yang cycle MTN proteins is likely an evolutionarily conserved mechanism whereby HopAF1 orthologs from multiple plant pathogens contribute to disease in a large variety of plant hosts.