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A recessive mutation in the Arabidopsis SSI2 gene confers SA‐ and NPR1 ‐independent expression of PR genes and resistance against bacterial and oomycete pathogens
Author(s) -
Shah Jyoti,
Kachroo Pradeep,
Nandi Ashis,
Klessig Daniel F.
Publication year - 2001
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1046/j.1365-313x.2001.00992.x
Subject(s) - npr1 , biology , mutant , pseudomonas syringae , systemic acquired resistance , gene , genetics , arabidopsis , natriuretic peptide , medicine , heart failure
Summary The Arabidopsis thaliana NPR1 gene is required for salicylic acid (SA)‐induced expression of pathogenesis‐related ( PR ) genes and systemic acquired resistance. However, loss‐of‐function mutations in NPR1 do not confer complete loss of PR gene expression or disease resistance. Thus these responses also can be activated via an NPR1‐independent pathway that currently remain to be elucidated. The ssi2‐1 mutant, identified in a genetic screen for suppressors of npr1‐5 , affects signaling through the NPR1‐independent defense pathway(s). In comparison with the wild‐type ( SSI2 NPR1 ) plants and the npr1‐5 mutant ( SSI2 npr1‐5 ), the ssi2‐1 npr1‐5 double mutant and the ssi2‐1 NPR1 single mutant constitutively express PR genes [ PR‐1 , BGL2 ( PR‐2 ) and PR‐5 ]; accumulate elevated levels of SA; spontaneously develop lesions; and possess enhanced resistance to a virulent strain of Peronospora parasitica . The ssi2‐1 mutation also confers enhanced resistance to Pseudomonas syringae pv. tomato ( Pst ); however, this is accomplished primarily via an NPR1‐dependent pathway. Analysis of ssi2‐1 NPR1 nahG and ssi2‐1 npr1‐5 nahG plants revealed that elevated SA levels were not essential for the ssi2‐1 ‐conferred phenotypes. However, expression of the nahG transgene did reduce the intensity of some ssi2‐1 ‐conferred phenotypes, including PR‐1 expression, and disease resistance. Based on these results, SSI2 or an SSI2‐generated signal appears to modulate signaling of an SA‐dependent, NPR1‐independent defense pathway, or an SA‐ and NPR1‐independent defense pathway.