Two Mol Plants reveal new mechanisms by which CAMTA transcription factors participate in regulating plant immune response.

Through complex perception and regulation network, plants resist the infection of various pathogenic microorganisms in the growth process.when vegetative and semi vegetative pathogens infect plants, plants recognize the pathogen infection, induce the expression of ics1 (isochorismate synthese 1, the major rate limiting enzyme of salicylic acid (SA) biosynthesis, and stimulate SA biosynthesis.SA further activates the expression of many downstream defense genes through receptor NPR1.under normal conditions, NPR1 exists in the cytoplasm as a polymer through intermolecular disulfide bond connection; when plants recognize pathogen invasion and induce SA synthesis, intracellular redox potential changes, resulting in the reduction of disulfide bond and the formation of NPR1 monomer. NPR1 monomer will enter the nucleus and interact with transcription factors such as TGA to stimulate the expression of defense genes [1, 2】。in addition, these SA regulated defense genes will be induced to express in uninfected leaves to prevent the spread of pathogens and prepare for future pathogen infection.this strong defense response is called systemic acquired resistance (SAR).pipecolic acid (PIP) and n-hydroxypipecolic acid (NHP) are involved in the regulation of SAR.in addition, ald1 (agd2 like defense response protein 1) and FMO1 (flavin dependent monooxygenase 1) are key catalytic enzymes in the biosynthesis of PIP and NHP, and these two enzymes are strongly induced by pathogen infection [3].camta (calmodulin binding transcription activator) transcription factor is a key regulator of SA mediated plant immunity.Arabidopsis contains six camta genes (camta1-camta6).among them, camta1, camta2 and camta3 are redundant in plant immunity.Arabidopsis camta1, camta2 and camta3 (camta1 / 2 / 3) inhibit SA synthesis and immune gene expression.in camta1 camta2 camta3 mutants, ics1 was highly induced, accompanied by the accumulation of SA and the enhancement of disease resistance.camta123 protein directly inhibits the expression of ics1 and ics1 positive regulatory factors (including cbp60g, sard1, EDS1 and PAD4) through binding with promoter [4,5]. However, little is known about the regulatory mechanism of camta1 / 2 / 3 on plant immunity.recently, molecular plant published online a paper entitled Arabidopsis camta transcription factors regularize piperic acid biosynthesis and priming of immunity genes by Michael thomashow research group of Michigan State University in the United States and Xin Li research group of University of British Columbia in Canada entitled redundant Camta transcription factors negatively regulate the biosynthesis of salicylic acid and n-hydroxypeptic acid by modulating the expression of sard1 and cbp60g.two studies reported that camta1 / 2 / 3 protein is involved in the regulation of plant immune response.the research team of Michael F. Thomas showed that the negative regulation of camta1 / 2 / 3 on plant immune gene expression depends on the inhibition of SA biosynthesis. camta1 / 2 / 3 deficiency can induce ald1 expression and promote PIP biosynthesis, which is independent of the increase of SA biosynthesis. camta123 with high PIP content had significantly increased SA and sag contents. At the same time, exogenous PIP treatment significantly increased the expression of ics1 and its positive regulatory factors cbp60g, sard1, PAD4 and EDS1 in Arabidopsis thaliana, which indicated that the loss of camta123 function led to PIP mediated SA biosynthesis. in addition, this study found that NPR1 protein level is dependent on the high level of PIP accumulation, and NPR1 plays an important role in PIP mediated biosynthesis of PIP, NHP and SA, as well as the induction of immune related genes. this study proposes a working model: in normal plants, camta123 binds to the promoters of cbp60g and sard1 and inhibits the expression of these genes; however, after infection, the function of camta1 / 2 / 3 is inhibited, and the expression of cbp60g and sard1 is increased, thus inducing the expression of ics1, ald1 and FMO1 and promoting SA, The biosynthesis of PIP and NHP leads to the induced expression of defense genes. in addition, PIP / NHP was transported to the uninfected distal leaves, resulting in the increase of NPR1 protein level and the increase of cell sensitivity to low endogenous SA. Meanwhile, NPR1 mediated ics1, ald1 and FMO1 gene expression were induced, which promoted the biosynthesis of SA, PIP and NHP and the initiation of SAR. working model for how loss of camta123 expression results in the induction of plant defense genes and SAR Xin Li research team found that cbp60g is a direct target gene of camta3. The autoimmunity of camta3 mutant was inhibited by sard1 / cbp60g double mutant and NHP synthesis deficient mutant ald1 and FMO1. interestingly, by screening the inhibitors of camta1 / 2 / 3 three mutants, various mutants blocking SA or NHP biosynthesis or signal transduction were obtained. These mutants can almost completely inhibit the autoimmunity of camta1 / 2 / 3. this indicates that SA and NHP pathways can be mutually amplified. this study proposed a working model of camta1 / 2 / 3 negatively regulating SA and NHP biosynthesis: camta1 / 2 / 3 repeatedly negatively regulated sard1 and cbp60g expression, thus reducing SA and NHP biosynthesis. the positive feedback regulation between SA and NHP signaling pathways promotes the enhancement of plant immune response. [1] Wu, Y., Zhang, D., Chu, J.Y., Boyle, P., Wang, y, Y., brindle, I.D., De Luca, v., and desppres, C. (2012) the Arabidopsis NPR1 protein is a receptor for the plant defense healthcare acid, cell Rep. 1: 639-647. [1] Wu, Y., Zhang, D., Chu, J.Y., Boyle, P., Wang, Y., Y., brindle, I.D., De Luca, v., and desppres, C. (2012), 2012) the Arabidopsis NPR1 protein is a receptor for the plant defense hormone oxalic acid, cell Rep. 1:639-647 [1:639-647], [1:639-647], [1:639-647], [1:639-647. [1:639-647 2] dewdney, J. Reuber, T.L., Wildermuth, M.C., Devoto, A., Cui, J.P., Stutius, L.M.,  Drummond, E.P., and Ausubel, F.M.  (2000). Three unique mutants of  Arabidospis identify eds loci required for limiting growth of a biotrophic fundal pathogen. Plant J. 24 :205-218.【3】Bernsdorff, F., Doring, A.C., Gruner, K., Schuck, S., Brautigam, A., and Zeier, J.(2016). Pipecolic acid orchestrates plant systemic acquired resistance and defense priming via salicylic acid-dependent and -independent pathways. Plant Cell 28 :102-129.【4】Du, L., Ali, G.S., Simons, K.A., Hou, J., Yang, T., Reddy, A.S., and Poovaiah, B.W.(2009). Ca(2+)/calmodulin regulates salicylic-acid-mediated plant immunity.  Nature 457 :1154-1158.【5】Kim, Y., Park, S., Gilmour, S.J., and Thomashow, M. F. (2013). Roles of camta transcription factors and salicylic acid in configuring the low temperature transcript and freezing tolerance of Arabidopsis. Plant J. 75: 364-376