Emerging concept for the role of photorespiration as an important part of abiotic stress response

Abstract

When plants are exposed to stress, generation of reactive oxygen species (ROS) is often one of the first responses. In order to survive, cells attempt to down-regulate the production of ROS, while at the same time scavenging ROS. Photorespiration is now appreciated as an important part of stress responses in green tissues for preventing ROS accumulation. Photorespiratory reactions can dissipate excess reducing equivalents and energy either directly (using ATP, NAD(P)H and reduced ferredoxin) or indirectly (e.g., via alternative oxidase (AOX) and providing an internal CO2 pool). Photorespiration, however, is also a source of H2 O2 that is possibly involved in signal transduction, resulting in modulation of gene expression. We propose that photorespiration can assume a major role in the readjustment of redox homeostasis. Protection of photosynthesis from photoinhibition through photorespiration is well known. Photorespiration can mitigate oxidative stress under conditions of drought/water stress, salinity, low CO2 and chilling. Adjustments to even mild disturbances in redox status, caused by a deficiency in ascorbate, AOX or chloroplastic NADP-malate dehydrogenase, comprise increases in photorespiratory components such as catalase, P-protein of glycine decarboxylase complex (GDC) and glycine content. The accumulation of excess reducing equivalents or ROS in plant cells also affects mitochondria. Therefore, a strong interaction between the chloroplast redox status and photorespiration is not surprising, but highlights interesting properties evident in plant cells. We draw attention to the fact that a complex network of multiple and dynamic systems, including photorespiration, prevents oxidative damage while optimising photosynthesis. Further experiments are necessary to identify and validate the direct targets of redox signals among photorespiratory components.

Lack of FTSH4 Protease Affects Protein Carbonylation, Mitochondrial Morphology, and Phospholipid Content in Mitochondria of Arabidopsis: New Insights into a Complex Interplay

“…The finding of several mitochondrial enzymes of photorespiration being highly carbonylated (GDC-T, SHM1, and MTLPD1) combined with the decreased abundance of other photorespiration enzymes (GLDP1 and GLDP2) suggests that this process is at least slowed down in ftsh4 mitochondria (Tables I and II). Since photorespiration is considered to be important to prevent ROS accumulation (Voss et al, 2013), the postulated decreased activity of the GDH/SHMT complex could be an additional cause for oxidative stress in ftsh4. Furthermore, among the proteins carbonylated preferentially in ftsh4 is the manganese superoxide dismutase, a key enzyme for eliminating mitochondrial superoxide radicals (Wang et al, 2010).…”

Stress-Induced Chloroplast Degradation in Arabidopsis Is Regulated via a Process Independent of Autophagy and Senescence-Associated Vacuoles

“…In addition, a wheat (Triticum aestivum) stay-green mutant (tasg1) displays delayed chlorophyll turnover and improved tolerance to drought because of the enhanced stability of thylakoid membranes (Tian et al, 2013). The stable chloroplasts also could contribute to maintain photorespiration, which has been shown to increase tolerance to abiotic stress by protecting the photosynthetic apparatus from oxidative damage and optimizing photosynthesis (Rivero et al, 2009;Voss et al, 2013). Here, we showed that silencing of CV increased chloroplast stability and prevented premature senescence under salt, oxidative, and drought stress ( Figure 5; Supplemental Figures 9B and 10).…”

Photorespiration Is Crucial for Dynamic Response of Photosynthetic Metabolism and Stomatal Movement to Altered CO 2 Availability

“…Therefore, PR metabolism is of vital importance for all oxygenic photosynthetic organisms (Eisenhut et al, 2008;Bauwe et al, 2012), as documented by the observation that cyanobacterial, green algal, and plant mutants in this pathway can only survive in an atmosphere with elevated CO 2 levels (Somerville and Ogren, 1979;Somerville, 2001;Nakamura et al, 2005;Voll et al, 2006;Engel et al, 2007;Schwarte and Bauwe, 2007;Eisenhut et al, 2008;Timm et al, 2011). Besides its metabolic repair function in the removal of the Rubisco's oxygenation product 2PG and carbon salvage, PR metabolism has also been suggested to protect from photoinhibition (Heber and Krause, 1980;Osmond, 1981;Kozaki and Takeba, 1996;Takahashi et al, 2007;Voss et al, 2013). PR is crucial for maintaining the activity of the CBB cycle, since it prevents both the accumulation of enzymeinhibiting metabolites (Anderson, 1971;Kelly and Latzko, 1976;Norman and Colman, 1991) and the depletion of intermediates from the CBB cycle.…”