期刊
PLANT JOURNAL
卷 57, 期 1, 页码 109-119出版社
WILEY
DOI: 10.1111/j.1365-313X.2008.03669.x
关键词
Arabidopsis thaliana; Pseudomonas syringae; disease resistance; AvrRps4; RPS4; TTC13
资金
- Millikan Endowment
- UM System Research Board [RB 06-004]
- US Department of Agriculture National Research Initiative [2002-35319-12639]
- National Science Foundation [IOS-0715926]
- Missouri Agricultural Experiment Station [MO-PSSL0603]
Effector-triggered immunity provides plants with strong protection from pathogens. However, this response has the potential to be highly deleterious to the host and needs to be tightly controlled. The molecular mechanisms in the plant that regulate the balance between activation and suppression of resistance are not fully understood. Previously, we identified Arabidopsis suppressor of rps4-RLD 1 (srfr1) mutants with enhanced resistance to the bacterial effector AvrRps4. These mutants were recessive and retained full susceptibility to virulent bacteria, suggesting that SRFR1 functions as a negative regulator and that AvrRps4-triggered immunity was specifically enhanced in the mutants. Consistent with this, we show here that the response to flagellin, an elicitor of basal resistance, is unaltered in srfr1-1. In contrast, resistance to AvrRps4 in srfr1-1 requires EDS1, a central regulator of effector-triggered immunity via multiple resistance genes. SRFR1 is a single-copy gene encoding a pioneer tetratricopeptide repeat protein conserved between plants and animals. The SRFR1 tetratricopeptide repeat domain shows sequence similarity to those of transcriptional repressors in Saccharomyces cerevisiae and Caenorhabditis elegans. Indeed, a sub-pool of SRFR1 transiently expressed in Nicotiana benthamiana leaf cells localizes to the nucleus. Identification of SRFR1 may therefore provide insight into the regulation of the transcriptional reprogramming that is activated by effector-triggered immunity.
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