Abstract
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 of Arabidopsis. edr mutants of Arabidopsis have 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 of RPW 8.1, and RPW 8.2 leading to HR, or SHL, and resistance. Bj NPR1 gene activates SAR to confer broad spectrum resistance to powdery mildew of B. juncea. At ROP regulated At RLCK V1 A3 has a role in basal resistance to powdery mildews. The At MLO2, At MLO6, and At MLO12 triple mutants are resistance to G. orontii. CPR5 controls resistance to powdery mildews, and PCD in response to infection by E. cruciferarum. There is a role of WRKY transcription factors, and over expression of R-genes like PMR, MLO, PEN, EDR, MAPK, MAPK 65-3, NPR1, PAD3, PAD4, ED5, SNARE, RLCKs, and KDL (At CEP1) to confer R to powdery mildews of crucifers. Higher levels of camalexin contribute to the enhanced R to powdery mildew in Cyp83 a1-3 mutants of Arabidopsis. SR1 plays a critical role in powdery mildew resistance by regulating EIN3, and NDR1 expression. There is harmonous coordination between transcriptional regulation, and resistance to powdery mildews. The application of Trichoderma harzianum and 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 genes EDS1, PAD4, and SAG (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. In Arabidopsis, R to PM is polygenic, and based on R-gene RPW8 or on combination of RPW 8 gene complex loci. Powdery mildew resistance genes of Arabidopsis have 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 by WRKY 18, WRKY 40 transcription factor of Arabidopsis, and enhances upon G. orontii infection to confer resistance. Transfer of powdery mildew resistance to B. oleracea from B. carinata through embryo rescue has been confirmed. Major gene sources of resistance against powdery mildew of crucifers have been identified.
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Saharan, G.S., Mehta, N.K., Meena, P.D. (2019). Host Resistance. In: Powdery Mildew Disease of Crucifers: Biology, Ecology and Disease Management. Springer, Singapore. https://doi.org/10.1007/978-981-13-9853-7_7
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