VASCULAR ASSOCIATED DEATH1, a Novel GRAM Domain–Containing Protein, Is a Regulator of Cell Death and Defense Responses in Vascular Tissues

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.

TheArabidopsis thaliana Myo-Inositol 1-Phosphate Synthase1 Gene Is Required forMyo-inositol Synthesis and Suppression of Cell Death

“…Like Meng et al (2009), we found that spontaneous cell death and the formation of lesions on leaves of mips1 mutants paralleled the progressive decline of myo-inositol in mips1 mutants throughout development (Figure 8) and can be rescued by myo-inositol supplementation (see Supplemental Figure 6 online). Overall, the mips1 mutants share characteristics with other lesion-mimic mutants (Lorrain et al, 2003) in that light potentiates the development of lesions (Bowling et al, 1997;Jambunathan et al, 2001;Lorrain et al, 2004), and the overall gene expression pattern is similar to lesion mimics as well as plants exposed to abiotic stress (Meng et al, 2009). Meng et al (2009) also noted a dependence on salicyclic acid (SA) synthesis for lesion formation in mips1 mutants and a reduction in the galactinol levels, which requires myo-inositol for synthesis and has been speculated to function as a general ROS scavenger.…”

Regulation of preprocambial cell state acquisition by auxin signaling inArabidopsisleaves

“…CYCA2;1 (Burssens et al, 2000), SCL3 (Ckurshumova et al, 2009), CESA2 (Beeckman et al, 2002)] and those with a proposed role in vascular development [e.g. VAN3 (SFC) (Deyholos et al, 2000;Koizumi et al, 2000), VAD1 (Lorrain et al, 2004), VND4 (Kubo et al, 2005)] or auxin response [e.g. ARF2 (Li et al, 2004), AXR3 (IAA17) (Rouse et al, 1998), HAT2 (Sawa et al, 2002)].…”

The Transcription Factors WRKY11 and WRKY17 Act as Negative Regulators of Basal Resistance in Arabidopsis thaliana

“…Plant inoculations and in planta bacterial growth analysis were performed essentially as described previously (Lorrain et al, 2004) using six to eight replicate plants per experiment. For the determination of disease symptoms and in planta bacterial growth, we used an inoculum of 10 5 cfu/mL for Pst DC3000 and of 2 3 10 5 cfu/mL for Pst DC3000 (avrRpt2).…”