**1. Introduction**

The characterization of a large set of photorespiratory mutants from a broad collection of phototrophs revealed photorespiration as an essential partner for oxygenic photosynthesis [1–6]. The photorespiratory pathway represents the only way to metabolize the Rubisco oxygenation reaction product 2-phosphoglycolate (2-PG; [7]) into the Calvin–Benson (CB) cycle intermediate 3-phosphoglycerate (3-PGA). Impairment of photorespiration causes 2-PG accumulation that leads to sequestration of C and Pi, severely impeding the biosynthesis of phosphorylated intermediates and triose phosphate export from the chloroplast. 2-PG has also direct inhibitory effects on CB cycle and glycolytic enzymes [8–11]. Hence, efficient 2-PG degradation through photorespiration is particularly important for photosynthesis in the presence of O2.

Despite its essential nature, the decarboxylation of glycine in the photorespiratory pathway leads to considerable losses of freshly assimilated carbon. The magnitude of these losses depends mainly on the CO2 and O2 partial pressures in the chloroplast, which can dramatically change under unfavorable environmental conditions, such as high light intensity, drought and high temperatures [12–14]. It is obvious that the photorespiratory flux needs to operate at higher speed in response to such conditions in order to cope with the higher 2-PG amounts. Given the CO2 loss during 2-PG recycling, plant research, however, aims to circumvent photorespiration in order to reduce carbon and energy losses [15–17]. In contrast, several reports demonstrated that an elevated flux through photorespiration could also increase photosynthesis under laboratory and field conditions [18–21] due to improved conversion of critical metabolites.

Apart from the central role of photorespiration supporting photosynthetic CO2 fixation, it has been suggested that it plays also a role in the stress response of plants. For example, malfunctioning of photorespiration leads to an enhanced susceptibility of the plants against pathogen attack [22,23], and lowered tolerance towards abiotic stresses [24–27]. This is mainly because photorespiration serves as alternative energy sink under unfavorable environmental conditions regenerating ADP and NADP and, thus, decreases acceptor limitation of the light process and related ROS formation [26,28,29]. Hence, high photorespiratory flux could help to prevent the chloroplastidal electron transport chain from overreduction and, finally, photoinhibition [24]. Interestingly, NADH-dependent hydroxypyruvate reductase 1 (HPR1) protein expression significantly increases in response to water-limiting conditions [25]. This result implies that the induction of critical steps of photorespiration is a natural mechanism to enhance the metabolic flux through the pathway to dissipate excess energy under stress conditions. The efficiency of such defense mechanism might be intensified via parallel increases of the cyclic electron flow and alternative oxidase pathways [26,28,29]. Despite excess energy dissipation, it was shown intact photorespiration is required for proper stomatal regulation and as such more directly involved in stress adaptation [30–32].

Among the photorespiratory enzymes, PGLP plays a crucial role since the efficient removal of 2-PG is critical to avoid negative impacts on chloroplast function as has been demonstrated by the high oxygen sensitivity of *PGLP* knock out and knock down mutants [10]. Therefore, we aimed to gain insights if faster 2-PG removal due to *PGLP* overexpression has an impact towards the acclimation to abiotic stresses. The results obtained are discussed with respect to 2-PG toxicity on carbon utilization and allocation and the potential of faster 2-PG degradation for acclimation to abiotic environmental stresses.
