Title of article :
VASCULAR ASSOCIATED DEATH1, a Novel GRAM Domain–Containing Protein, Is a Regulator of Cell Death and Defense Responses in Vascular Tissues
Author/Authors :
Lorrain، Severine نويسنده , , Lin، Baiqing نويسنده , , Auriac، Marie Christine نويسنده , , Kroj، Thomas نويسنده , , Saindrenan، Patrick نويسنده , , Nicole، Michel نويسنده , , Balague، Claudine نويسنده , , Roby، Dominique نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2004
Pages :
-2216
From page :
2217
To page :
0
Abstract :
The hypersensitive response (HR) is a programmed cell death that is commonly associated with plant disease resistance. A novel lesion mimic mutant, vad1 (for vascular associated death1), that exhibits light conditional appearance of propagative HR-like lesions along the vascular system was identified. Lesion formation is associated with expression of defense genes, production of high levels of salicylic acid (SA), and increased resistance to virulent and avirulent strains of Pseudomonas syringae pv tomato. Analyses of the progeny from crosses between vad1 plants and either nahG transgenic plants, sid1, nonexpressor of PR1 (npr1), enhanced disease susceptibility1 (eds1), or non-race specific disease resistance1 (ndr1) mutants, revealed the vad1 cell death phenotype to be dependent on SA biosynthesis but NPR1 independent; in addition, both EDS1 and NDR1 are necessary for the proper timing and amplification of cell death as well as for increased resistance to Pseudomonas strains. VAD1 encodes a novel putative membrane-associated protein containing a GRAM domain, a lipid or protein binding signaling domain, and is expressed in response to pathogen infection at the vicinity of the hypersensitive lesions. VAD1 might thus represent a new potential function in cell death control associated with cells in the vicinity of vascular bundles.
Keywords :
N deposition , Indicator species , Ectomycorrhizae , Oligotrophic soils , Pine barrens
Journal title :
THE PLANT CELL
Serial Year :
2004
Journal title :
THE PLANT CELL
Record number :
113292
Link To Document :
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