Access

You are not currently logged in.

Access your personal account or get JSTOR access through your library or other institution:

login

Log in to your personal account or through your institution.

If You Use a Screen Reader

This content is available through Read Online (Free) program, which relies on page scans. Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.

Oligogalacturonide-Auxin Antagonism Does Not Require Posttranscriptional Gene Silencing or Stabilization of Auxin Response Repressors in Arabidopsis

Daniel V. Savatin, Simone Ferrari, Francesca Sicilia and Giulia De Lorenzo
Plant Physiology
Vol. 157, No. 3 (November 2011), pp. 1163-1174
Stable URL: http://www.jstor.org/stable/41435580
Page Count: 12
  • Read Online (Free)
  • Subscribe ($19.50)
  • Cite this Item
Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Oligogalacturonide-Auxin Antagonism Does Not Require Posttranscriptional Gene Silencing or Stabilization of Auxin Response Repressors in Arabidopsis
Preview not available

Abstract

α-4-Linked oligogalacturonides (OGs) derived from plant cell walls are a class of damage-associated molecular patterns and well-known elicitors of the plant immune response. Early transcript changes induced by OGs largely overlap those induced by flg22, a peptide derived from bacterial flagellin, a well-characterized microbe-associated molecular pattern, although responses diverge over time. OGs also regulate growth and development of plant cells and organs, due to an auxin-antagonistic activity. The molecular basis of this antagonism is still unknown. Here we show that, in Arabidopsis (Arabidopsis thaliana), OGs inhibit adventitious root formation induced by auxin in leaf explants as well as the expression of several auxin-responsive genes. Genetic, biochemical, and pharmacological experiments indicate that inhibition of auxin responses by OGs does not require ethylene, jasmonic acid, and salicylic acid signaling and is independent of RESPIRATORY BURST OXIDASE HOMOLOGUE D-mediated reactive oxygen species production. Free indole-3-acetic acid levels are not noticeably altered by OGs. Notably, OG-as well as flg22-auxin antagonism does not involve any of the following mechanisms: (1) stabilization of auxin-response repressors; (2) decreased levels of auxin receptor transcripts through the action of microRNAs. Our results suggest that OGs and flg22 antagonize auxin responses independently of Aux/Indole-3-Acetic Acid repressor stabilization and of posttranscriptional gene silencing.

Page Thumbnails

  • Thumbnail: Page 
1163
    1163
  • Thumbnail: Page 
1164
    1164
  • Thumbnail: Page 
1165
    1165
  • Thumbnail: Page 
1166
    1166
  • Thumbnail: Page 
1167
    1167
  • Thumbnail: Page 
1168
    1168
  • Thumbnail: Page 
1169
    1169
  • Thumbnail: Page 
1170
    1170
  • Thumbnail: Page 
1171
    1171
  • Thumbnail: Page 
1172
    1172
  • Thumbnail: Page 
1173
    1173
  • Thumbnail: Page 
1174
    1174