Plants interact with the dynamic environment constantly. Photorespiration is a physiological process that occurs simultaneously with photosynthesis and is often considered wasteful. However, photorespiration involves the coordination of multiple organelles and connects with various primary metabolic pathways, thus its response to the environment greatly influences the fate of plants. The roles of photorespiration in plant interaction with the dynamic environment are still not very clear. To investigate the underlying mechanisms, I applied various strategies to dissect the roles of photorespiration in plant response to both abiotic and biotic environmental factors. Previous studies from my lab found that some Arabidopsis photorespiratory mutants only exhibit obvious photosynthetic phenotypes under high and dynamic light conditions, suggesting that photorespiration is regulated by high light. To identify potential modulators of photorespiration under such conditions, I performed a genetic screen for suppressors of the Arabidopsis photorespiratory mutant, hpr1, which is defective in the peroxisomal hydroxypyruvate reductase 1. A suppressor that partially rescued the small rosette of the hpr1 mutant was mapped to GLYR1, which encodes the cytosolic glyoxylate reductase 1 that converts glyoxylate to glycolate. Independent loss-of-function alleles of GLYR1 also recapitulated the partial rescue of hpr1 in plant appearance and photosynthetic and photorespiratory activities. Interestingly, glyr1 also suppressed the phenotypes of the photorespiratory mutant catalase 2, but not a null allele of the PLGG1 (Plastidic Glycolate Glycerate Transporter 1) gene. Further investigations using metabolic and genetic tools provided evidence of a possible cytosolic glyoxylate shunt, which is triggered under high light conditions and in the absence of a properly functional main photorespiratory pathway. This shunt reduces the accumulated cytosolic glyoxylate to hydroxypyruvate, thus helping with carbon recycling through the cytosolic HPR2 enzyme. These findings support the metabolic flexibility of the photorespiration network under stress conditions. My transcriptomic analysis of hpr1 and its suppressor glyr1 hpr1 also supports the existence of this non-canonical cytosolic pathway. Drastic transcriptional reprogramming that involves broad cellular functions was found in the hpr1 mutant, which can be largely reverted by defective GLYR1. The rescuing effect of glyr1 is only prominent when HPR1 is absent, supporting the view that the accumulation of photorespiratory intermediates in hpr1 causes a stressful cellular environment that disrupts biological processes globally, and that glyr1 partially prevents this metabolic accumulation. To investigate the role of photorespiration in plant response to biotic stress, I analyzed the performance of photorespiratory mutants in plant immune response. My data showed that deficiencies of the peroxisomal photorespiratory enzyme HPR1 and the chloroplastic transporter PLGG1 compromised response in both layers of immunity, pattern-triggered immunity and effector-triggered immunity, and these defects can be rescued when the plants were grown under high CO2 conditions. These findings suggest that HPR1 and PLGG1 contribute to plant immune response via the photorespiratory pathway. My research broadens our understanding of the role of photorespiration in plants under stress conditions, which may help with agricultural efforts to improve crop performance in response to the changing environment.
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