Abstract
Resistance to biotrophic pathogens is largely dependent on the hormone salicylic acid (SA) while jasmonic acid (JA) regulates resistance against necrotrophs. JA negatively regulates SA and is, in itself, negatively regulated by SA. A key component of the JA signal transduction pathway is its receptor, the COI1 gene. Mutations in this gene can affect all the JA phenotypes, whereas mutations in other genes, either in JA signal transduction or in JA biosynthesis, lack this general effect. To identify components of the part of the resistance against biotrophs independent of SA, a mutagenised population of NahG plants (severely depleted of SA) was screened for suppression of susceptibility. The screen resulted in the identification of intragenic and extragenic suppressors, and the results presented here correspond to the characterization of one extragenic suppressor, coi1-40. coi1-40 is quite different from previously described coi1 alleles, and it represents a strategy for enhancing resistance to biotrophs with low levels of SA, likely suppressing NahG by increasing the perception to the remaining SA. The phenotypes of coi1-40 lead us to speculate about a modular function for COI1, since we have recovered a mutation in COI1 which has a number of JA-related phenotypes reduced while others are equal to or above wild type levels.
Highlights
The ability of plants to prevent pathogen colonization relies on a complex network of genes and phytohormones
Arabidopsis thaliana (Arabidopsis) plants with high levels of Salicylic acid (SA) are more resistant to pathogens such as the bacteria Pseudomonas syringae pv. tomato isolate DC3000 (Pto) [2], while plants with lower SA levels are less resistant to Pto and other pathogens [3]
The transgene was inserted between the genes At2g46970 and At2g46980, and there were no differences in susceptibility to Pto with other Col-0 or Ws-0 NahG lines
Summary
The ability of plants to prevent pathogen colonization relies on a complex network of genes and phytohormones. Salicylic acid (SA) is a well known hormone essential for activating plant basal defence responses, against biotrophic pathogens (reviewed by [1]). It has been shown that transgenic plants expressing the salicylate hydroxylase gene from Pseudomonas putida (NahG) can rapidly degrade SA [3] and are more susceptible to biotrophic pathogens [4] such as Pto [5]. SA resistance triggers a number of defence or pathogenesis-related genes including PR1. This gene is widely used as a marker for biotic stress and is required for various types of resistance, including Systemic Acquired Resistance (SAR). Considering the array of resistance responses to biotrophs, there is evidence for part of the resistance response being independent of SA [7]
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