Molecular genetic analysis of cell death and defense signaling in Arabidopsis hrl1 mutant.

摘要

Defense against pathogens in Arabidopsis is orchestrated by at least three signaling molecules: salicylic acid (SA), jasmonic acid (JA), and ethylene (ET). The hrl1 (for h&barbelow;ypersensitive r&barbelow;esponse-like l&barbelow;esions 1) mutant of Arabidopsis is characterized by spontaneous necrotic lesions, accumulation of reactive oxygen species (ROS), constitutive expression of SA- and ET/JA-responsive defense genes, and enhanced resistance to virulent bacterial and oomycete pathogens. Epistasis analyses of hrl1 with npr1, etr1, coi1, and SA-depleted nahG plants revealed novel interactions between SA and ET/JA signaling pathways in regulating PR gene expression and cell death. Northern analysis of the RNA isolated from the lesion+ (local) and the lesion − (systemic) leaves of double mutants of hrl1 uncovered different signaling requirements for the expression of defense genes in these tissues. Expression of ET/JA-responsive PDF1.2 gene was markedly reduced in hrl1 npr1 and in the SA-depleted hrl1 nahG plants. In hrl1 nahG plants, expression of PDF1.2 was regulated by benzathiadiazole (BTH) in a concentration dependent manner: induced at low concentration and suppressed at high concentration. The hrl1 etr1 plants lacked systemic PR-1 expression, and exhibited compromised resistance to virulent Pseudomonas syringae. Inhibiting JA responses in hrl1 coil plants lead to exaggerated cell death and severe stunting of plants. Finally, the hrl1 mutation led to elevated expression of AtrbohD, which encodes a major sub-unit of the NADPH oxidase complex. These results indicate that cell death and defense induction in hrl1 is regulated synergistically by SA and ET/JA defense pathways.; The preexisting defense responses enable hrl1 plants to resist virulent pathogen infection. Pre-treating Arabidopsis wild-type plants with SAR-inducers, prior to pathogen infection resulted in a significant decrease in HR cell death. The suppressed HR cell death and the failure to enhance PR gene expression following avirulent pathogen infection in hrl1 suggest that the preexisting defense responses serve as negative feedback loops to regulate extensive cell death and defense-related gene expression. In hrl1, the chronic stress response due to PR gene expression may alter the cellular physiology at various nodes that lead to insensitivity to subsequent pathogen attack. Down-regulation of HR cell death in the presence of an already existing systemic resistance response may be a way for plants to prevent excessive cell death and further defense induction. (Abstract shortened by UMI.)