Published by Oxford University Press [2008] on behalf of the Society for Experimental Biology.
Preface
The concept that reactive oxygen species (ROS) damage plant tissues is not new, but over the last decade or so increasing evidence has emerged that redox signalling plays an important role in plant development and plant responses to stress. For example, redox signals have now been implicated as central components to floral development, sensing cell carbohydrate status, and responses to pathogen attack, high salinity, drought, and high light stress. Studies on animal and fungal systems have confirmed that, like plants, nitric oxide and hydrogen peroxide are important signals, and other ubiquitous redox elicitors may soon be identified.
There are several technical difficulties that hamper progress with the identification of redox signalling pathways in all biological systems. Firstly, redox signals are likely to be strong oxidants or reductants and therefore tend to react quickly within cells. Given that they have a short half-life, it is likely that they are generated and sensed within the same cell or tissues. This combination makes the design and interpretation of experiments difficult as the ROSs are generated ex situ, and then react with unintended target sites as they penetrate into the organs and tissues. Secondly, it is difficult to separate the responses that arise from redox-mediated damage from those that arise from redox elicitors evoking specific signalling cascades.
The idea for a session on ‘Redox Signalling in Plants’ at the 2007 SEB Conference in Glasgow emerged from the growing number of reports on the topic, and from the perception that, at least for hydrogen peroxide and nitric oxide, the basic cellular mechanisms for their synthesis were well understood; what was now required was a focus on the mechanisms by which synthesis was activated, the specific targets of the signals, and how cross-talk between different signalling pathways modulates response. Unfortunately, since that time it has emerged that we still know of only one mechanism for NO production in plants (that mediated by nitrate reductase); after two false starts the identity of an authentic plant NO-synthase still remains contentious. The Plant Redox Signalling session ran for two full days and included talks on NO- and H2O2-mediated responses to plant pathogen attack, the role of cell redox state in response to high light and cation stress, the effects of redox mediators on plant growth and metabolism, and novel approaches for identifying signalling targets.
This Focus Section commissioned by the Journal for Experimental Botany contains a series of papers from the symposium. Phil Mullineaux and colleagues present their ongoing work on high light-activated genes that appear to be mediated through a H2O2 signal, whilst Graham Noctor and colleagues addresses the thorny issue of why reported H2O2 levels are so variable. Gary Loake and colleagues provide a review of the role of NO signalling in plant disease resistance and recent attempts to identify the target proteins that become nitrosylated. David Wendehenne and associates present evidence that NO can evoke Ca2+ signalling responses and, in addition, kinase activity can be modulated by nitrosylation. Steve Neill and co-workers present their most recent findings on NO signalling in regulating stomatal function. Finally, Jörg Durner and colleagues provide details of a DNA microarray bioinformatics approach to identify transcription factors and their associated promoter elements that are activated by NO.
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