Characterization Of An Arabidopsis Glutaredoxin That Interacts With Core Components Of The Salicylic Acid Signal Transduction Pathway – Its Role In Regulating The Jasmonic Acid Pathway

نویسندگان

  • Ivan Ndamukong
  • Christiane Gatz
  • Ivo Feußner
  • Gerhard Braus
  • Benjamin Fode
  • Ivan Che Ndamukong
چکیده

Salicylic acid (SA) is a plant signalling molecule that mediates the induction of defense responses upon attack by a variety of pathogens. Activation sequence-1 (as-1) type cis elements and their cognate basic/leucine zipper (bZIP)-type transcription factors of the TGA family regulate transcription in response to SA and in response to xenobiotic chemicals. TGA factors interact with NPR1 (NON EXPRESSOR OF PR GENES 1), a central regulator of many SA-induced defense responses. Changes in the redox state of both TGA1 and NPR1 have been observed under inducing conditions. In order to identify further proteins interacting with TGA factors, a yeast protein interaction screen with tobacco TGA2.2 as a bait and an Arabidopsis thaliana cDNA prey library was performed and led to the identification of a member of the glutaredoxin family (GRX480, encoded by At1g28480). Glutaredoxins are candidates for mediating redox regulation of proteins because of their capacity to catalyze disulfide transitions. Transgenic Arabidopsis plants ectopically expressing GRX480 show wild-type expression of standard marker genes for SAand xenobiotic-inducible expression. However, jasmonic acid (JA)-inducible transcription of defensin gene PDF1.2 is suppressed in these plants. As SA is known to interfere with JA-dependent transcription, GRX480, which is induced after SA-treatment, may constitute one of the regulatory compounds controlling PDF1.2 promoter activity. In contrast to the NPR1-mediated antagonism between SAand JA-dependent signal transduction networks described earlier, the GRX480-mediated repression does not affect expression of other JA-inducible genes like ERF1, LOX2 and VSP indicating that NPR1 and GRX480 act through separate pathways.

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تاریخ انتشار 2006