Frontiers in Plant Science (Mar 2015)

Proteome readjustments in the apoplastic space of Arabidopsis thaliana ggt1 mutant leaves exposed to UV-B radiation

  • Anna Rita eTrentin,
  • Micaela ePivato,
  • Micaela ePivato,
  • Syed Muhammad Muntazir Mehdi,
  • Leonard Ebinezer Barnabas,
  • Sabrina eGiaretta,
  • Marta eFabrega-Prats,
  • Dinesh ePrasad,
  • Dinesh ePrasad,
  • Giorgio eArrigoni,
  • Giorgio eArrigoni,
  • Antonio eMasi

DOI
https://doi.org/10.3389/fpls.2015.00128
Journal volume & issue
Vol. 6

Abstract

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Ultraviolet-B radiation acts as an environmental stimulus, but in high doses it has detrimental effects on plant metabolism. Plasma membranes represent a major target for ROS generated by this harmful radiation. Oxidative reactions occurring in the apoplastic space are counteracted by antioxidative systems mainly involving ascorbate and, to some extent, glutathione. The occurrence of the latter and its exact role in the extracellular space are not well documented, however. In Arabidopsis thaliana, the gamma-glutamyl transferase isoform GGT1 bound to the cell wall takes part in the so-called gamma-glutamyl cycle for extracellular glutathione degradation and recovery, and may be implicated in redox sensing and balance.In this work, oxidative conditions were imposed with UV-B and studied in redox altered ggt1 mutants. The response of ggt1 knockout Arabidopsis leaves to UV-B radiation was assessed by investigating changes in extracellular glutathione and ascorbate content and their redox state, and in apoplastic protein composition. Our results show that, on UV-B exposure, soluble antioxidants respond to the oxidative conditions in both genotypes. Rearrangements occur in their apoplastic protein composition, suggesting an involvement of H2O2, which may ultimately act as a signal. Other important changes relating to hormonal effects, cell wall remodeling, and redox activities are discussed. We argue that oxidative stress conditions imposed by UV-B and disruption of the gamma-glutamyl cycle result in similar stress-induced responses, to some degree at least.

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