Host Resistance
Host Resistance
复制标题
DOI：
10.1007/978-981-13-9853-7_7
复制
发表时间：
2019
期刊：
影响因子：
--
通讯作者：
G. S. Saharan;N. Mehta;P. Meena
中科院分区：
文献类型：
--
作者：
G. S. Saharan;N. Mehta;P. Meena
十字花科植物对白粉病的抗性是多层次的，在渗透前和渗透后阶段都是多组分的。复杂的免疫应答通过ROS、H2 O2的积累、胼胝质、果胶、纤维素、蜡、硅的沉积、离子流、乳突的形成、细胞壁并置、酚类化合物、R基因的过表达、PR蛋白、蛋白磷酸化、植物抗毒素的生物合成、真菌酶抑制剂、壳聚糖八聚体、HR的触发、SAR的诱导和非宿主抗性机制而进化。这些细胞骨架成分在十字花科植物对白粉病病原菌的抗性中具有非常重要和关键的功能和结构作用。防御通过SA信号传导以及乙烯和茉莉酸（JA）的同时感知被激活。十字花科植物-白粉病寄主致病系统中几个抗病基因的过量表达诱导了寄主的抗病性。MLO基因编码的7个跨膜钙调素结合蛋白赋予拟南芥适应白粉病的广谱抗性。拟南芥的突变体在SA介导的抗性、线粒体功能和程序性细胞死亡之间存在普遍联系。PMR突变体通过改变宿主细胞壁组成而赋予对白粉病的抗性。SA增加可增强RPW 8.1和RPW 8.2的表达，导致HR或SHL和抗性。BjNPR 1基因激活SAR赋予B. Juncea。At ROP调节At RLCK V1 A3在对白粉病的基础抗性中起作用。At MLO 2、At MLO 6和At MLO 12三重突变体均对G. orontii具有抗性，其中CPR 5控制对白粉病的抗性，PCD控制对E.十字花科植物。WRKY转录因子和抗病基因如PMR、MLO、PEN、EDR、MAPK、MAPK 65-3、NPR 1、PAD 3、PAD 4、ED 5、SNARE、RLCK和KDL（At CEP 1）的过度表达对十字花科白粉病具有抗病性。在Cyp 83 a1- 3突变体中，较高水平的Camalexin有助于提高抗病性，SR 1通过调控EIN 3和NDR 1的表达在白粉病抗性中起重要作用。转录调控与抗白粉病之间存在着协调一致的关系。哈茨戊木霉及其CF在十字花科蔬菜中诱导（ISR）抗性的应用十字花科植物非寄主抗病基因对白粉病的作用机制尚未完全阐明，但抗病性强、持久。非寄主抗病性在入侵前由PEN基因介导，入侵后由EDS 1、PAD 4和SAG（101）基因控制。在甘蓝中，对白粉病的抗性受一对带有修饰基因的显性基因控制。HC-1和PCC-2的抗病基因均为单基因控制，表现完全显性。在拟南芥中，R到PM是多基因的，并且基于R基因RPW 8或RPW 8基因复合位点的组合。将拟南芥的抗白粉病基因定位在第II（RPW 1）、第III（RPW 2、RPW 3、RPW 7、RPW 8）、第IV（RPW 4）和第V（RPW 5、RPW 6）染色体上。在油菜籽中，γ射线诱变植物由于具有18个碳原子的不饱和脂肪酸浓度的增加而表现出对白粉病的抗性。硫代葡萄糖苷和Camalexin的诱导在十字花科植物抗白粉病中起重要作用。拟南芥WRKY 18、WRKY 40转录因子影响Camalexin的生物合成和积累，在G.使其产生耐药性。白粉病抗性向B.甘蓝carinatathrough.
Host resistance in crucifers to powdery mildews is multilayered, and multi-components both at pre- and post-penetration stages. The intricate immune responses are evolved through accumulation of ROS, H2O2, deposition of callose, pectin, cellulose, waxes, silicon, ion fluxes, formation of papilla, cell wall apposition, phenolic compounds, over expression of R-genes, PR proteins, protein phosphorylation, biosynthesis of phytoalexins, fungal enzymes inhibiters, chito-octamers, triggering of HR, induction of SAR, and non-host resistance mechanisms. These cytoskeleton components have very important and crucial functional, and structural roles in host resistance to powdery mildew pathogens of crucifers. Defenses are activated either through SA signaling, and simultaneous perception of ethylene, and jasmonic acid (JA). The over expression of several R-genes in crucifers –powdery mildew host pathosystem induces host resistance. MLO genes encoding seven-trans-membrane, calmodulin-binding protein confers broad spectrum resistance to adapted powdery mildews ofArabidopsis. edrmutants ofArabidopsishave a general link between SA mediated resistance, mitochondrial function, and programmed cell death. pmr mutants confer resistance to powdery mildew through altered cell wall composition of host. Increased SA enhances the expression ofRPW 8.1, andRPW 8.2leading to HR, or SHL, and resistance. BjNPR1gene activates SAR to confer broad spectrum resistance to powdery mildew ofB. juncea. At ROP regulated At RLCK V1 A3 has a role in basal resistance to powdery mildews. TheAt MLO2,At MLO6, andAt MLO12triple mutants are resistance to G.orontii.CPR5controls resistance to powdery mildews, and PCD in response to infection byE. cruciferarum. There is a role of WRKY transcription factors, and over expression of R-genes likePMR, MLO, PEN, EDR, MAPK, MAPK 65-3, NPR1, PAD3, PAD4, ED5, SNARE, RLCKs, andKDL(At CEP1) to confer R to powdery mildews of crucifers. Higher levels of camalexin contribute to the enhanced R to powdery mildew inCyp83 a1-3mutants ofArabidopsis.SR1 plays a critical role in powdery mildew resistance by regulatingEIN3, andNDR1expression. There is harmonous coordination between transcriptional regulation, and resistance to powdery mildews. The application ofTrichoderma harzianumand its CF induces (ISR) resistance in crucifers. Mechanisms of non-host R in crucifers to powdery mildews have been unrevealed which is strong and durable. Non-host resistance is PEN-gene-mediated at pre- invasion, and controlled by genesEDS1, PAD4, andSAG(101) at post-invasion of powdery mildew pathogens. In cabbage, R to powdery mildew is controlled by a single dominant gene with modifiers. A single R gene controls R to powdery mildew in HC-1, and PCC-2 with complete dominance. InArabidopsis, R to PM is polygenic, and based on R-geneRPW8or on combination ofRPW8 gene complex loci. Powdery mildew resistance genes ofArabidopsishave been mapped on chromosomes II (RPW1), III (RPW2, RPW3, RPW7, RPW8), IV (RPW4), and V (RPW 5, RPW 6). In rapeseed gamma rays mutagenic plants exhibit R to powdery mildew due to an increase in concentration of unsaturated fatty acids with 18 carbon atoms. Induction of glucosinolates, and camalexin plays important roles for resistance to powdery mildew of crucifers. Camalexin biosynthesis, and accumulation are affected byWRKY 18, WRKY 40transcription factor ofArabidopsis, and enhances uponG. orontiiinfection to confer resistance. Transfer of powdery mildew resistance toB. oleraceafromB. carinatathrough …