The thesis discusses the basic mechanisms of plant immunity, with emphasis on systemic acquired resistance (SAR). It presents the perception of molecular patterns by cell-surface receptors in pattern-triggered immunity (PTI) and the detection of pathogen effectors by intracellular receptors in effector-triggered immunity (ETI). Receptor activation initiates calcium signalling, the activation of mitogen-activated protein kinases (MAP kinases), the production of reactive oxygen species, changes in defence gene expression and local responses, including the hypersensitive response. Receptor function is illustrated by the resistance of tobacco against tobacco mosaic virus, in which the N immune receptor, together with the plant protein NRIP1, detects the viral protein p50 and restricts virus spread. A local infection can also induce SAR in distant tissues. Its establishment involves salicylic acid, pipecolic acid, N-hydroxypipecolic acid, jasmonates and other signalling molecules, which together establish a primed state of defence. The thesis also addresses the effects of defence on plant growth, its interactions with abiotic stress and the possibilities of using chemical elicitors and beneficial microorganisms in plant protection. These approaches act mainly preventively, while their effectiveness depends on the dose, timing of application, plant genotype, environmental conditions and infection pressure. Therefore, they are most suitable as a component of integrated plant protection.
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