Variations on a theme: Non-canonical mechanisms of effector-triggered immunity

Abstract

Effector-triggered immunity (ETI) can be defined as immune responses activated upon specific recognition of a pathogen effector protein by its cognate plant immune receptor protein. This classic gene-for-gene model of the interaction of one pathogen effector, also known as an Avirulence (Avr) gene, with one plant immune receptor gene, known as a Resistance (R) gene has been documented since the 1950s. Since then, different types of recognition that deviate from the gene-for-gene model, for example, immune receptor pairs and immune receptor networks, have been identified. In addition, while many R genes encode NLR (nucleotide binding, leucine rich repeat) proteins, R genes that encode only parts of NLR domains, and non-NLR encoding R genes such as tandem kinases have been identified, broadening the immune receptor repertoire in plants. In recent years, there have been significant advances in understanding the molecular mechanisms of NLR intracellular immune receptors in plants, including how they are inhibited, activated, and regulated. This review covers recent developments in ETI initiation mechanisms and in plant NLR biology.