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Molecular Mechanisms of Host Resistance to Hemibiotrophs and Necrotrophs

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Molecular Mechanism of Crucifer’s Host-Resistance

Abstract

The molecular mechanisms of nonhost resistance to Alternaria in Brassica indicated activation of defense-related genes earlier in nonhost plants than the host plants. Six QTLs governing resistance to Alternaria brassicae have been identified, five of them are population-specific while one QTL is common between all the three mapping populations. In Brassica, defense-related genes (PR proteins) including defensins (β-glucanases and chitinases) have been identified against Alternaria. Different defensin genes in B. juncea have been characterized for their structures, evolution, cellular location, and regulation in response to SA, JA, and Alternaria infection. Chitinase genes in Brassica have been identified to breed Alternaria-resistant cultivars. A single R-locus RCH-1 has been identified at the tip of chromosomes 4 in Arabidopsis thaliana ecotype Eil-O against Colletotrichum higginsianum. The locus RCHz maps to an extensive cluster of R-loci known as MRC-J in the Arabidopsis ecotype Ws-O. In B. oleracea, two types of R-genes have been identified. A type with single dominant genes is effective against Fusarium race 1 and stable under high or low temperatures. B type is polygenic resistance, and it is unstable under high temperature above 24 °C. Type A resistance to FOC 1 race 1 conferred by a dominant single gene, FOC1, has been mapped and molecular markers have been developed. R-genes and QTLs have been identified from B. rapa, B. juncea, B. nigra, and B. napus to provide resistance to Leptosphaeria. The LepR1 and lepR2 genes provide cotyledon and adult plant resistance in B. napus to Leptosphaeria. The genetic background is useful markers to select the most suitable genotype as a recipient parent while developing Brassica cvs. with Lm resistance. The combined effect of R-genes and host genetic background generates stronger defense responses through induction of genes related to callose deposition, upregulation of ROS, and SA and JA pathways.

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Saharan, G.S., Mehta, N.K., Meena, P.D. (2021). Molecular Mechanisms of Host Resistance to Hemibiotrophs and Necrotrophs. In: Molecular Mechanism of Crucifer’s Host-Resistance. Springer, Singapore. https://doi.org/10.1007/978-981-16-1974-8_3

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