NPR1: the spider in the web of induced resistance signaling pathways

Abstract

The plant hormones salicylic acid (SA), jasmonic acid (JA), and ethylene (ET) are major players in the regulation of signaling networks that are involved in induced defense responses against pathogens and insects. During the past two years, significant progress has been made in understanding the function of NON-EXPRESSOR OF PATHOGENESIS-RELATED GENES1 (NPR1), a key regulator of systemic acquired resistance (SAR), that is essential for transducing the SA signal to activate PATHOGENESIS-RELATED (PR) gene expression. SA-mediated redox changes in Arabidopsis cells regulate both the functioning of NPR1 and its binding to TGA1, a member of the TGA family of transcription factors that activate SA-responsive elements in the promoters of PR genes upon binding with NPR1. Apart from its role in regulating SAR in the nucleus, a novel cytosolic function of NPR1 in cross-communication between SA- and JA-dependent defense signaling pathways has been identified. Other advances in induced resistance signaling, such as the implication that ET is involved in the generation of systemic signal molecules, the suggestion of the involvement of lipid-derived molecules in long-distance signaling, and the identification of new components of various systemic defense signaling pathways, shed new light on how plants actively defend themselves against harmful organisms.

coi1, coronatine insensitive1; DIR1, DEFECTIVE IN INDUCED RESISTANCE1; ERF1, ETHYLENE RESPONSE FACTOR1; ET, ethylene; ISR, induced systemic resistance; JA, jasmonic acid; nahG, salicylate hydroxylase gene; NIM1, NON-INDUCIBLE IMMUNITY1; NPR1, NON-EXPRESSOR OF PATHOGENESIS-RELATED GENES1; PI, proteinase inhibitor; PR, PATHOGENESIS-RELATED; ROI, reactive oxygen intermediates; SA, salicylic acid; SABP2, SA-BINDING PROTEIN2; SAR, systemic acquired resistance; SCFCOI1, SKP1, CDC53p/CUL1 F-boxCOI1; TMV, Tobacco mosaic virus