Novel regulators in photosynthetic redox control of plant metabolism and gene expression.

Reduction-oxidation (redox) reactions are an essential part of cell metabolism and represent a major fraction of all catabolic and anabolic reactions. Their dominant characteristic is that they generate and consume compounds with in part highly negative redox potential. Redox reactions occur at many sites in the cell, e.g. in membranes such as thylakoids, plastid envelope, and plasma membrane and in aqueous cell phases such as the stroma, thylakoid lumen, and cytosol. Electron transport systems in cell membranes, particularly in the photosynthetic and respiratory electron transport chains, employ diverse redox cofactors such as iron-sulfur (FeS) clusters and quinones and also excitable systems in photosynthesis that all can generate reactive oxygen species (ROS). The redox state of the aqueous phase is dominated by soluble redox metabolites, which include NAD(P)H, glutathione, and e.g. metabolite pairs such as malate and oxaloacetate, and in addition thiol/disulfide proteins (Foyer and Noctor, 2009). The redox potential of a compound is a relative attribute and defines its propensity to donate electrons to another compound within a given redox couple. The process of electron transfer is directed from the compound with more to that with the less negative redox potential. By this means redox reactions largely determine the thermodynamics of the energetic fluxes in living cells. However, the electron transfer within a redox couple needs to be strictly controlled to avoid the unintended electron transfer to other substrates with a relative positive redox potential. Oxygen represents such a compound and electron transfer to it can generate potentially harmful ROS. To balance redox metabolism and minimize ROS or reactive nitrogen species (RNS) formation, cells operate a redox signaling network. The network senses environmentally induced redox imbalances and initiates compensatory responses either to readjust redox homeostasis or to repair oxidative damage. Basically, the network consists of redox input elements, redox transmitters, redox targets, and redox sensors (Dietz, 2008). The basic structure and many components of the thiol-disulfide redox regulatory network are conserved among all cells and most cell compartments. The significance of this network is well established for some pathways, but still emergent for additional functions due to the ongoing identification of novel redox targets. Lindahl and Kieselbach provided a comprehensive inventory of the experimentally identified disulfide proteomes of the chloroplast (Lindahl and Kieselbach, 2009). As part of the Plant Physiology Focus Issue on Plastid Biology, this Update focuses on plastid redox regulation as an example for the basic principles of redox regulation in metabolism. In addition, the function of recently identified new players in plastid redox regulation is described.