Plant immune receptor decoy: Pathogens in their own trap

Microbial pathogens have evolved sophisticated strategies to infect their hosts, often resulting in disease. The host, in turn, can produce novel proteins (receptors or antibodies) that recognize pathogen molecules to trigger defense. Unlike animals, plants do not possess any adaptive immunity to defend themselves against pathogens. Therefore, they rely entirely on their genetic resistance capability (innate immunity) conferred by a family of receptors expressed in individual cells. The plant innate immune system can be divided into two layers of defense. The first, known as pattern-triggered immunity (PTI) leading to basal defense, involves the recognition of microbe-associated molecular patterns (MAMPs) by corresponding plasma membrane pattern-recognition receptors (PRRs). PTI can be suppressed by specific pathogen virulence factors (known as effectors). To detect such pathogen molecules or their interference with host proteins, plants have evolved a second layer of defense, known as effector-triggered immunity (ETI) [1]. ETI is mediated by intracellular nucleotide-binding–leucine-rich repeat receptors (NLRs) that resemble mammalian NLRs [2]. The speed with which microbial populations can produce new effectors places enormous pressure on plant hosts to fight back with genetically new or altered receptor recognition modes.