SR1, a Calmodulin-Binding Transcription Factor, Modulates Plant Defense and Ethylene-Induced Senescence by Directly Regulating NDR1 and EIN3      

Abstract

Plant defense responses are tightly controlled by many positive and negative regulators to cope with attacks from various pathogens. Arabidopsis (Arabidopsis thaliana) ENHANCED DISEASE RESISTANCE2 (EDR2) is a negative regulator of powdery mildew resistance, and edr2 mutants display enhanced resistance to powdery mildew (Golovinomyces cichoracearum). To identify components acting in the EDR2 pathway, we screened for edr2 suppressors and identified a gain-of-function mutation in SIGNAL RESPONSIVE1 (SR1), which encodes a calmodulin-binding transcription activator. The sr1-4D gain-of-function mutation suppresses all edr2-associated phenotypes, including powdery mildew resistance, mildew-induced cell death, and ethylene-induced senescence. The sr1-4D single mutant is more susceptible to a Pseudomonas syringae pv tomato DC3000 virulent strain and to avirulent strains carrying avrRpt2 or avrRPS4 than the wild type. We show that SR1 directly binds to the promoter region of NON-RACE-SPECIFIC DISEASE RESISTANCE1 (NDR1), a key component in RESISTANCE TO PSEU-DOMONAS SYRINGAE2-mediated plant immunity. Also, the ndr1 mutation suppresses the sr1-1 null allele, which shows enhanced resistance to both P. syringae pv tomato DC3000 avrRpt2 and G. cichoracearum. In addition, we show that SR1 regulates ethylene-induced senescence by directly binding to the ETHYLENE INSENSITIVE3 (EIN3) promoter region in vivo. Enhanced ethylene-induced senescence in sr1-1 is suppressed by ein3. Our data indicate that SR1 plays an important role in plant immunity and ethylene signaling by directly regulating NDR1 and EIN3.

BR-SIGNALING KINASE1 Physically Associates with FLAGELLIN SENSING2 and Regulates Plant Innate Immunity in Arabidopsis

“…Consistent with previous findings, edr2 accumulated more H 2 O 2 than the wild type at 2 DAI; however, this high level of H 2 O 2 accumulation was suppressed by the bsk1-1 mutation ( Figure 1D). In addition to the enhanced resistance to powdery mildew, the edr2 mutant displays increased ethylene-induced senescence phenotypes, indicating possible crosstalk between defense responses and senescence (Tang et al, 2005;Nie et al, 2012). To investigate whether bsk1-1 affects edr2-mediated ethylene-induced senescence, we treated edr2 bsk1-1 with ethylene for 3 d and assessed the leaf senescence.…”

Recent Advances in Calcium/Calmodulin-Mediated Signaling with an Emphasis on Plant-Microbe Interactions

“…It was also shown that AtSR1/CAMTA3 interacts with a CGCG box motif in the 21-kb promoter region of EDS1 both in vivo and in vitro and suppresses the transcription of EDS1, a critical player in the SA activation loop and toll interleukin 1 receptor-nucleotide binding domain (NB)-leucine rich repeat (LRR)-type R gene-mediated defense in Arabidopsis (Du et al, 2009). Recently, AtSR1/CAMTA3 was also shown to negatively regulate ethylene-mediated senescence by recognizing a CGCG box in the promoters of EIN3 and disease resistance by interacting with a CGCG box in the promoters of NDR1, a key signaling component required for coiled-coil-NB-LRR-type R gene-mediated plant immunity (Nie et al, 2012). Similar to the function of CAMTA3, OsCBT, a CAMTA member from rice, also plays a negative role in regulating rice defense against both the bacterial pathogen Xanthomonas oryzae pv oryzae and the rice blast fungus Magnaporthe grisea (Koo et al, 2009).…”

CAMTA-Mediated Regulation of Salicylic Acid Immunity Pathway Genes in Arabidopsis Exposed to Low Temperature and Pathogen Infection

“…Other than this difference, each Arabidopsis CAMTA protein has four functional domains positioned in the same relative order from the N-to C-terminal end (Rahman et al, 2016): the CG-1 DNA binding domain, an ankyrin (ANK) repeat domain, an IQ domain composed of two IQ motifs, and a CaM binding (CaMB) domain. Both the IQ and CaMB domains bind CaM in a calcium-dependent manner (Bouché et al, 2002;Choi et al, 2005;Du et al, 2009;Nie et al, 2012).…”