3
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Melatonin as a regulator of plant ionic homeostasis: implications for abiotic stress tolerance

      , , ,
      Journal of Experimental Botany
      Oxford University Press (OUP)

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Melatonin is a highly conserved and ubiquitous molecule that operates upstream of a broad array of receptors in animal systems. Since melatonin was discovered in plants in 1995, hundreds of papers have been published revealing its role in plant growth, development, and adaptive responses to the environment. This paper summarizes the current state of knowledge of melatonin’s involvement in regulating plant ion homeostasis and abiotic stress tolerance. The major topics covered here are: (i) melatonin’s control of H+-ATPase activity and its implication for plant adaptive responses to various abiotic stresses; (ii) regulation of the reactive oxygen species (ROS)–Ca2+ hub by melatonin and its role in stress signaling; and (iii) melatonin’s regulation of ionic homeostasis via hormonal cross-talk. We also show that the properties of the melatonin molecule allow its direct scavenging of ROS, thus preventing negative effects of ROS-induced activation of ion channels. The above ‘desensitization’ may play a critical role in preventing stress-induced K+ loss from the cytosol as well as maintaining basic levels of cytosolic Ca2+ required for optimal cell operation. Future studies should focus on revealing the molecular identity of transporters that could be directly regulated by melatonin and providing a bioinformatic analysis of evolutionary aspects of melatonin sensing and signaling.

          Related collections

          Most cited references221

          • Record: found
          • Abstract: found
          • Article: not found
          Is Open Access

          ROS Are Good.

          Reactive oxygen species (ROS) are thought to play a dual role in plant biology. They are required for many important signaling reactions, but are also toxic byproducts of aerobic metabolism. Recent studies revealed that ROS are necessary for the progression of several basic biological processes including cellular proliferation and differentiation. Moreover, cell death-that was previously thought to be the outcome of ROS directly killing cells by oxidation, in other words via oxidative stress-is now considered to be the result of ROS triggering a physiological or programmed pathway for cell death. This Opinion focuses on the possibility that ROS are beneficial to plants, supporting cellular proliferation, physiological function, and viability, and that maintaining a basal level of ROS in cells is essential for life.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Contrasting mechanisms of defense against biotrophic and necrotrophic pathogens.

            It has been suggested that effective defense against biotrophic pathogens is largely due to programmed cell death in the host, and to associated activation of defense responses regulated by the salicylic acid-dependent pathway. In contrast, necrotrophic pathogens benefit from host cell death, so they are not limited by cell death and salicylic acid-dependent defenses, but rather by a different set of defense responses activated by jasmonic acid and ethylene signaling. This review summarizes results from Arabidopsis-pathogen systems regarding the contributions of various defense responses to resistance to several biotrophic and necrotrophic pathogens. While the model above seems generally correct, there are exceptions and additional complexities.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              NADPH oxidase AtrbohD and AtrbohF genes function in ROS-dependent ABA signaling in Arabidopsis.

              Reactive oxygen species (ROS) have been proposed to function as second messengers in abscisic acid (ABA) signaling in guard cells. However, the question whether ROS production is indeed required for ABA signal transduction in vivo has not yet been addressed, and the molecular mechanisms mediating ROS production during ABA signaling remain unknown. Here, we report identification of two partially redundant Arabidopsis guard cell-expressed NADPH oxidase catalytic subunit genes, AtrbohD and AtrbohF, in which gene disruption impairs ABA signaling. atrbohD/F double mutations impair ABA-induced stomatal closing, ABA promotion of ROS production, ABA-induced cytosolic Ca(2+) increases and ABA- activation of plasma membrane Ca(2+)-permeable channels in guard cells. Exogenous H(2)O(2) rescues both Ca(2+) channel activation and stomatal closing in atrbohD/F. ABA inhibition of seed germination and root elongation are impaired in atrbohD/F, suggesting more general roles for ROS and NADPH oxidases in ABA signaling. These data provide direct molecular genetic and cell biological evidence that ROS are rate-limiting second messengers in ABA signaling, and that the AtrbohD and AtrbohF NADPH oxidases function in guard cell ABA signal transduction.
                Bookmark

                Author and article information

                Contributors
                (View ORCID Profile)
                Journal
                Journal of Experimental Botany
                Oxford University Press (OUP)
                0022-0957
                1460-2431
                September 30 2022
                September 30 2022
                May 30 2022
                September 30 2022
                September 30 2022
                May 30 2022
                : 73
                : 17
                : 5886-5902
                Article
                10.1093/jxb/erac224
                35640481
                8be85157-488a-47b8-9fe1-4849144cf012
                © 2022

                https://academic.oup.com/pages/standard-publication-reuse-rights

                History

                Comments

                Comment on this article