New mutants provide clues into regulation of systemic acquired resistance

When plants encounter pathogens, resistance mechanisms are activated that can prevent infection, aid recovery from disease and prevent future infection. An important component in a plant’s defense arsenal is the pathogen-induced response called systemic acquired resistance (SAR), which when activated can prevent infection by a wide range of pathogens. SAR was described in 1961 by Frank Ross (Cornell University, USA) and later found by others to be associated with the induction of a suite of pathogenesis-related (PR) genes and their corresponding proteins. Salicylic acid is an endogenous signaling molecule, which is required for the induction of SAR. Application of salicylic acid or its synthetic analogs [2,6-dichloroisonicotinic acid (INA) or benzo (1,2,3)thiadiazole-7-carbothioic acid S-methyl ester (BTH)] to plants induces PR gene expression and resistance as would a biological agent. In addition, transgenic plants that express salicylate hydroxylase, which is encoded by the bacterial nahG gene, can neither accumulate salicylic acid after pathogen attack, nor activate SAR (reviewed in 1 Ryals J. et al. Systemic acquired resistance. Plant Cell. 1996; 8: 1809-1819 Crossref PubMed Scopus (1743) Google Scholar , 2 Delaney T.P. Genetic dissection of acquired resistance to disease. Plant Physiol. 1997; 106: 5-12 Crossref Scopus (111) Google Scholar ). In the past several years, genetic analysis has revealed components in the pathway that regulates SAR by identifying mutants perturbed in this response. The recent description of a suppressor mutation that restores function to SAR mutants, and the cloning of its gene, has generated new insights into how this important plant defense response is regulated 3 Li X. et al. Identification and cloning of a negative regulator of systemic acquired resistance, SNI1, through a screen for suppressors of npr1-1.. Cell. 1999; 98: 329-339 Abstract Full Text Full Text PDF PubMed Scopus (202) Google Scholar .