
Silicon‐mediated resistance of A rabidopsis against powdery mildew involves mechanisms other than the salicylic acid ( SA )‐dependent defence pathway
Author(s) -
Vivancos Julien,
Labbé Caroline,
Menzies James G.,
Bélanger Richard R.
Publication year - 2015
Publication title -
molecular plant pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.945
H-Index - 103
eISSN - 1364-3703
pISSN - 1464-6722
DOI - 10.1111/mpp.12213
Subject(s) - arabidopsis , powdery mildew , salicylic acid , biology , mutant , priming (agriculture) , defence mechanisms , phenotype , microbiology and biotechnology , gene , transporter , heterologous , arabidopsis thaliana , plant disease resistance , plant defense against herbivory , genetics , botany , germination
Summary On absorption by plants, silicon ( S i) offers protection against many fungal pathogens, including powdery mildews. The mechanisms by which S i exerts its prophylactic role remain enigmatic, although a prevailing hypothesis suggests that S i positively influences priming. Attempts to decipher S i properties have been limited to plants able to absorb S i, which excludes the model plant A rabidopsis because it lacks S i influx transporters. In this work, we were able to engineer A rabidopsis plants with an S i transporter from wheat ( TaLsi1 ) and to exploit mutants ( pad4 and sid2 ) deficient in salicylic acid ( SA )‐dependent defence responses to study their phenotypic response and changes in defence expression against G olovinomyces cichoracearum ( G c ) following S i treatment. Our results showed that TaLsi1 plants contained significantly more S i and were significantly more resistant to G c infection than control plants when treated with S i, the first such demonstration in a plant transformed with a heterologous S i transporter. The resistant plants accumulated higher levels of SA and expressed higher levels of transcripts encoding defence genes, thus suggesting a role for S i in the process. However, TaLsi1 pad4 and TaLsi1 sid2 plants were also more resistant to G c than were pad4 and sid2 plants following S i treatment. Analysis of the resistant phenotypes revealed a significantly reduced production of SA and expression of defence genes comparable with susceptible controls. These results indicate that S i contributes to Arabidopsis defence priming following pathogen infection, but highlight that S i will confer protection even when priming is altered. We conclude that S i‐mediated protection involves mechanisms other than SA ‐dependent defence responses.