Nitric oxide modulates ozone-induced cell death, hormone biosynthesis and gene expression in Arabidopsis thaliana

Authors

  • Reetta Ahlfors,

    Corresponding author
    1. Plant Biology, Department of Biological and Environmental Sciences, University of Helsinki, PO Box 65 (Viikinkaari 1), FI-00014 Helsinki, Finland
    Search for more papers by this author
  • Mikael Brosché,

    Corresponding author
    1. Plant Biology, Department of Biological and Environmental Sciences, University of Helsinki, PO Box 65 (Viikinkaari 1), FI-00014 Helsinki, Finland
    Search for more papers by this author
  • Hannes Kollist,

    Corresponding author
    1. Plant Biology, Department of Biological and Environmental Sciences, University of Helsinki, PO Box 65 (Viikinkaari 1), FI-00014 Helsinki, Finland
    2. Institute of Technology, University of Tartu, Nooruse 1, Tartu 50411, Estonia
    Search for more papers by this author
  • Jaakko Kangasjärvi

    1. Plant Biology, Department of Biological and Environmental Sciences, University of Helsinki, PO Box 65 (Viikinkaari 1), FI-00014 Helsinki, Finland
    Search for more papers by this author
    • These authors contributed equally to this work.


(fax +358 9 19159552; e-mail jaakko.kangasjarvi@helsinki.fi).

Summary

Nitric oxide (NO) is involved together with reactive oxygen species (ROS) in the activation of various stress responses in plants. We have used ozone (O3) as a tool to elicit ROS-activated stress responses, and to activate cell death in plant leaves. Here, we have investigated the roles and interactions of ROS and NO in the induction and regulation of O3-induced cell death. Treatment with O3 induced a rapid accumulation of NO, which started from guard cells, spread to adjacent epidermal cells and eventually moved to mesophyll cells. During the later time points, NO production coincided with the formation of hypersensitive response (HR)-like lesions. The NO donor sodium nitroprusside (SNP) and O3 individually induced a large set of defence-related genes; however, in a combined treatment SNP attenuated the O3 induction of salicylic acid (SA) biosynthesis and other defence-related genes. Consistent with this, SNP treatment also decreased O3-induced SA accumulation. The O3-sensitive mutant rcd1 was found to be an NO overproducer; in contrast, Atnoa1/rif1 (Arabidopsis nitric oxide associated 1/resistant to inhibition by FSM1), a mutant with decreased production of NO, was also O3 sensitive. This, together with experiments combining O3 and the NO donor SNP suggested that NO can modify signalling, hormone biosynthesis and gene expression in plants during O3 exposure, and that a functional NO production is needed for a proper O3 response. In summary, NO is an important signalling molecule in the response to O3.

Ancillary