TY - JOUR
T1 - S-nitrosylation of AtSABP3 antagonizes the expression of plant immunity
AU - Wang, Yi-Qin
AU - Feechan, Angela
AU - Yun, Byung-Wook
AU - Shafiei, Reza
AU - Hofmann, Andreas
AU - Taylor, Paul
AU - Xue, Peng
AU - Yang, Fu-Quan
AU - Xie, Zhen-Sheng
AU - Pallas, Jacqueline A.
AU - Chu, Cheng-Cai
AU - Loake, Gary J.
PY - 2009/1
Y1 - 2009/1
N2 - Changes in cellular redox status are a well established response across phyla following pathogen challenge. In this context, the synthesis of nitric oxide (NO) is a conspicuous feature of plants responding to attempted microbial infection and this redox-based regulator underpins the development of plant immunity. However, the associated molecular mechanism(s) have not been defined. Here we show that NO accretion during the nitrosative burst promotes increasing S-nitrosylation of the Arabidopsis thaliana salicylic acid-binding protein 3 (AtSABP3) at cysteine (Cys) 280, suppressing both binding of the immune activator, salicylic acid (SA), and the carbonic anhydrase (CA) activity of this protein. The CA function of AtSABP3 is required for the expression of resistance in the host against attempted pathogen infection. Therefore, inhibition of AtSBAP3 CA function by S-nitrosylation could contribute to a negative feedback loop that modulates the plant defense response. Thus, AtSABP3 is one of the first targets for S-nitrosylation in plants for which the biological function of this redox-based post-translational modification has been uncovered. These data provide a molecular connection between the changes in NO levels triggered by attempted pathogen infection and the expression of disease resistance.
AB - Changes in cellular redox status are a well established response across phyla following pathogen challenge. In this context, the synthesis of nitric oxide (NO) is a conspicuous feature of plants responding to attempted microbial infection and this redox-based regulator underpins the development of plant immunity. However, the associated molecular mechanism(s) have not been defined. Here we show that NO accretion during the nitrosative burst promotes increasing S-nitrosylation of the Arabidopsis thaliana salicylic acid-binding protein 3 (AtSABP3) at cysteine (Cys) 280, suppressing both binding of the immune activator, salicylic acid (SA), and the carbonic anhydrase (CA) activity of this protein. The CA function of AtSABP3 is required for the expression of resistance in the host against attempted pathogen infection. Therefore, inhibition of AtSBAP3 CA function by S-nitrosylation could contribute to a negative feedback loop that modulates the plant defense response. Thus, AtSABP3 is one of the first targets for S-nitrosylation in plants for which the biological function of this redox-based post-translational modification has been uncovered. These data provide a molecular connection between the changes in NO levels triggered by attempted pathogen infection and the expression of disease resistance.
UR - http://www.scopus.com/inward/record.url?scp=59049098945&partnerID=8YFLogxK
U2 - 10.1074/jbc.M806782200
DO - 10.1074/jbc.M806782200
M3 - Article
C2 - 19017644
AN - SCOPUS:59049098945
SN - 0021-9258
VL - 284
SP - 2131
EP - 2137
JO - Journal of Biological Chemistry
JF - Journal of Biological Chemistry
IS - 4
ER -