Regulation of gene expression in response to salicylic acid

Abteilung "Molekularbiologie und Physiologie"

des Albrecht-von-Haller-Institutes für Pflanzenwissenschaften

Mitglied des Göttinger Zentrums für Molekulare Biowissenschaften

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Regulation of gene expression in response to salicylic acid

Salicylic acid (SA) is a plant hormone that is synthesized upon attack of plants by biotrophic pathogens. Salicylsäure

As a consequence of increased salicylic acid levels, a number of genes are induced that have either anti-microbial effects or that help to protect the cells against damage elicited by reactive oxygen species generated during the interaction or by microbial toxins. Plants that cannot accumulate salicylic acid lack this response show an enhanced susceptibility phenotype. Using Arabidopsis thaliana as a model system, Xinnian Dong and coworkers at Duke University have identified the central regulatory protein NPR1 as an indispensible component of SA-mediated resistance. The current working model suggests that NPR1 is localized in the cytosol under non-inducing conditions. Upon increased SA-levels, critical disulfide bridges are reduced allowing the protein to enter the nucleus. In the nucleus, NPR1 interacts with the TGA family of transcription factors. This interaction seems to be crucial for the subsequent activation of defense genes. In addition to this, a number of other TGA-dependent SA-regulated promoters are independent from NPR1. A common feature of the NPR1-independent promoters is the spacing between two binding sites for TGA factors, whereas NPR1-dependent promoters can have a variable distance (Krawczyk et al., 2002). We are elucidating how the critical spacing can connect the TGA factors to different regulatory signalling cascades.

During our search for TGA-interacting proteins that might play a role in NPR1-independent processes, we have identified a glutaredoxin, which is transcriptionally induced by salicylic acid (Ndamukong et al., 2007). Transgenic plants that constitutively express this glutaredoxin cannot induce the jasmonic acid-inducible PDF1.2 gene. Jasmonic acid is a crucial plant signalling molecule that orchestrates plant defense preocesses in response to necrotrophic pathogens and herbivore attack. It is well known that SA can suppress JA-elicited responses. Therefore, we hypothesize that transcriptional activation of the TGA interacting glutaredoxin by SA plays an important role in this negative cross-talk. Moreover, a certain subfamily of TGA factors needs to be reduced to become competent to interact with NPR1. At the moment, we are elucidating the function of the glutaredoxins in the various TGA-dependent processes (PhD Position available).

PhD students: Sebastian Pape (since 2005), Katja Rindermann (since 2005), Mark Zander (since 2007), Julia Köster (since 2007)

Publications: Krawczyk et al., 2002; Weigel et al., 2005; Ndamukong et al., 2007

Funding: DFG