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Chloroplasts play a pivotal role in the metabolism of leaf mesophyll cells, functioning as a cellular hub that orchestrates molecular reactions in response to environmental stimuli. These organelles contain complex protein machinery for energy conversion and are indispensable for essential metabolic pathways. Proteins located within the chloroplast envelope membranes facilitate bidirectional communication with the cell and connect essential pathways, thereby influencing acclimation processes to challenging environmental conditions such as temperature fluctuations and light intensity changes. Despite their importance, a comprehensive overview of the impact of envelope-located proteins during acclimation to environmental changes is lacking. Understanding the role of these proteins in acclimation processes could provide insights into enhancing stress tolerance under increasingly challenging environments. This review highlights the significance of envelope-located proteins in plant acclimation.
Chloroplasts play a pivotal role in the metabolism of leaf mesophyll cells, functioning as a cellular hub that orchestrates molecular reactions in response to environmental stimuli. These organelles contain complex protein machinery for energy conversion and are indispensable for essential metabolic pathways. Proteins located within the chloroplast envelope membranes facilitate bidirectional communication with the cell and connect essential pathways, thereby influencing acclimation processes to challenging environmental conditions such as temperature fluctuations and light intensity changes. Despite their importance, a comprehensive overview of the impact of envelope-located proteins during acclimation to environmental changes is lacking. Understanding the role of these proteins in acclimation processes could provide insights into enhancing stress tolerance under increasingly challenging environments. This review highlights the significance of envelope-located proteins in plant acclimation.
Sugar transport across membranes is critical for plant development and yield. However, an analysis of the role of intracellular sugar transporters in senescence is lacking. Here, we characterized the role of Senescence-Associated Sugar Transporter1 (SAST1) during senescence in Arabidopsis (Arabidopsis thaliana). SAST1 expression was induced in leaves during senescence and after the application of abscisic acid (ABA). SAST1 is a vacuolar protein that pumps glucose out of the cytosol. sast1 mutants exhibited a stay-green phenotype during developmental senescence, after the darkening of single leaves, and after ABA feeding. To explain the stay-green phenotype of sast1 mutants, we analyzed the activity of the glucose-induced master-regulator TOR (target of rapamycin), which is responsible for maintaining a high anabolic state. TOR activity was higher in sast1 mutants during senescence compared to wild types, whereas the activity of its antagonist, SNF1-related protein kinase 1 (SnRK1), was reduced in sast1 mutants under senescent conditions. This deregulation of TOR and SnRK1 activities correlated with high cytosolic glucose levels under senescent conditions in sast1 mutants. Although sast1 mutants displayed a functional stay-green phenotype, their seed yield was reduced. These analyses place the activity of SAST1 in the last phase of a leaf's existence in the molecular program required to complete its life cycle.
Sugars, produced through photosynthesis, are at the core of all organic compounds synthesized and used for plant growth and response to the environmental changes. Therefore, their production, transport and utilization is highly regulated and integrated throughout the plant life cycle. The maintenance of sugar partitioning between the different subcellular compartments (e.g., cytosol, vacuole, chloroplast), and mediated by different families of sugar transporters (e.g., SUC/SUT, SWEET, ERDL), is instrumental to adjust the photosynthesis performance and response to abiotic constraints. Here we investigated in Arabidopsis the consequences of the disruption of four genes coding for SWEET sugar transporters (SWEET11, SWEET12, SWEET16 and SWEET17) on plant photosynthesis and response to drought. Our results show that, the disruption of the intercellular sugar transport, mediated by SWEET11, negatively impacts photosynthesis efficiency and net CO2 assimilation while the stomatal conductance and transpiration are increased. These defects are accompanied by an impairment of both cytosolic and chloroplastic glycolysis leading to an accumulation of soluble sugars, starch and organic acids. Further, our results suggest that in the swt11swt12 mutant, the sucrose-induced feedback mechanism on stomatal closure is poorly efficient. On the other hand, changes in fructose partitioning in mesophyll and vascular cells, mediated by SWEET17, positively impact photosynthesis probably through an increased starch synthesis together with a higher vacuolar sugar storage. Finally, our work shows that, a fine tuning, at transcriptional and/or translational levels, of the expression of SWEET11, SWEET16 and SWEET17 is needed in order to properly respond to drought stress.
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