![]() ![]() ![]() INTRODUCTION: A CONTEMPORARY VIEW OF PLANT IMMUNITYĮarly in the 20th century, by performing genetic experiments, Harold Flor showed that inheritance of plant immunity to pathogens, as well as the ability of the pathogen to cause disease, is controlled by corresponding gene pairs ( Flor, 1942). We argue that plant resistance is determined by immune receptors that recognize appropriate ligands to activate defense, the amplitude of which is likely determined by the level required for effective immunity. Rather, as illustrated by examples provided here, there is a continuum between PTI and ETI. Therefore, we put forward that the distinction between PAMPs and effectors, between PAMP receptors and resistance proteins, and, therefore, also between PTI and ETI, cannot strictly be maintained. As effectors may elicit defense responses and PAMPs may be required for virulence, single components cannot exclusively be referred to by one of the two terms. For example, some effectors display wide distribution, while some PAMPs are rather narrowly conserved or contribute to pathogen virulence. However, not all microbial defense activators conform to the common distinction between PAMPs and effectors. Both types of molecule can trigger plant immunity, designated PAMP-triggered and effector-triggered immunity (PTI and ETI, respectively). Typically, pathogen-associated molecular patterns (PAMPs) are considered to be conserved throughout classes of microbes and to contribute to general microbial fitness, whereas effectors are species, race, or strain specific and contribute to pathogen virulence.
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