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The Arabidopsis gain‐of‐function mutant dll1 spontaneously develops lesions mimicking cell death associated with disease
Author(s) -
Pilloff Rachel K.,
Devadas Sendil K.,
Enyedi Alexander,
Raina Ramesh
Publication year - 2002
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.2002.01265.x
Subject(s) - pseudomonas syringae , mutant , arabidopsis , biology , hypersensitive response , npr1 , virulence , pathogen , plant disease resistance , salicylic acid , disease , programmed cell death , microbiology and biotechnology , genetics , function (biology) , phenotype , gene , medicine , heart failure , apoptosis , pathology , natriuretic peptide
Summary We describe the characterization of a novel gain‐of‐function Arabidopsis mutant, dll1 ( disease‐like lesions1 ), which spontaneously develops lesions mimicking bacterial speck disease and constitutively expresses biochemical and molecular markers associated with pathogen infection. Despite the constitutive expression of defense‐related responses, dll1 is unable to suppress the growth of virulent pathogens. However, dll1 elicits normal hypersensitive response in response to avirulent pathogens, thus indicating that dll1 is not defective in the induction of normal resistance responses. The lesion + leaves of dll1 support the growth of hrcC mutant of Pseudomonas syringae , which is defective in the transfer of virulence factors into the plant cells, and therefore non‐pathogenic to wild‐type Col‐0 plants. This suggests that dll1 intrinsically expresses many of the cellular processes that are required for pathogen growth during disease. Epistasis analyses reveal that salicylic acid and NPR1 are required for lesion formation, while ethylene modulates lesion development in dll1 , suggesting that significant overlap exist between the signalling pathways leading to resistance‐ and disease‐associated cell death. Our results suggest that host cell death during compatible interactions, at least in part, is genetically controlled by the plant and DLL1 may positively regulate this process.