A transcriptional regulator mediates the salicylic acid and Jasmonic acid/ethylene antagonism by modulating phosphoenolpyruvate shunt in Arabidopsis
W. MUCHERO (1) (1) Oak Ridge National Laboratory, U.S.A.

The antagonism between salicylic acid (SA) and jasmonic acid (JA)/ethylene (ET) signaling has major implications in the tradeoff between growth and defense against pathogens. Here, we propose that transcriptional modulation of carbon allocation between the shikimate and glycolysis pathways underlies this observed antagonism. Our model is based on the observation that phosphoenolpyruvate (PEP) is a precursor for pyruvate biosynthesis in the glycolysis pathway which subsequently leads to JA and ET biosynthesis. Similarly, PEP is a precursor for 3-deoxy-D-arabinoheptulosonate 7-phosphate (DAHP) biosynthesis in the shikimate pathway which leads to phenylpropanoid and SA biosynthesis. Competition for this shared precursor presents a tractable explanation for the mutual antagonism between these defense pathways. Our assertion was supported by observations that loss-of-function in a transcriptional regulator of the PEP shunt resulted in over 2-fold constitutive downregulation of defense-related genes AtWRKY22, AtWRKY26, AtWRKY33, AtWRKY40, AtWRKY53, AtNPR3 and ethylene response factors AtERF1, AtERF2, AtERF5, AtERF6, AtERF11, AtERF13, AtERF38, and AtERF104. Conversely, the loss-of-function mutant exhibited more than 2-fold constitutive upregulation of canonical transcription factors involved in phenylpropanoid biosynthesis, including MYB46, MYB55, MYB58, MYB63 and MYB103. These results suggest that PEP is preferentially shunted towards the shikimate pathway in the mutant lines. With this cumulative evidence, we propose that this transcription factor is a master regulator of the SA and JA/ET antagonism and implications of its loss of function on microbial community dynamics will be presented. 

Abstract Number: P16-461
Session Type: Poster