The novel chloroplast glucose transporter pGlcT2 affects adaptation to extended light periods
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PROVIDER: PRJNA925827 | ENA |
REPOSITORIES: ENA
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Project description:Intracellular sugar compartmentation is critically involved in plant development and acclimation to challenging environmental conditions. Sugar transport proteins are present in the plasma membrane and in membranes of organelles such as vacuoles, the Golgi apparatus and plastids. Here we report on a novel transporter of the Monosaccharide Transporter Family (MSF), that is the closest phylogenetic homolog to the chloroplast-localized glucose transporter pGlcT and that we therefore term plastidic glucose transporter 2 (pGlcT2). Its gene complemented glucose uptake deficiency of an Escherichia coli ptsG/manXYZ mutant strain and biochemical characterization revealed that this transporter specifically facilitates glucose transport, whereas other sugars do not serve as substrates. pGlcT2-GFP fusions located to the chloroplast envelope, and promoter activity analyses indicated that pGlcT2 is mainly produced in seedlings and in the rosette center of mature Arabidopsis plants. In the absence of additional sugars, pGlcT2-overexpression lines exhibited impaired germination. In conjunction with molecular and metabolic data we propose that pGlcT2 acts as a glucose importer that can limit cytosolic glucose availability in developing pGlcT2-overexpressing seedlings. Overexpression, as well as deletion of pGlcT2 resulted in impaired growth efficiency under long day and especially under continuous light conditions, suggesting that pGlcT2 contributes to a release of glucose derived from starch mobilization late in the light phase. These data thus indicate that the facilitator pGlcT2 changes its direction of glucose transport during plant development and suggest that the activity of pGlcT2 must be controlled spatially and temporarily, in order to prevent developmental defects during adaptation to periods of extended light.
2023-01-25 | GSE223330 | GEO
Project description:Intracellular sugar compartmentation is critical in plant development and acclimation to challenging environmental conditions. Sugar transport proteins are present in plasma membranes and in membranes of organelles such as vacuoles, the Golgi apparatus, and plastids. However, there may exist other transport proteins with uncharacterized roles in sugar compartmentation. Here we report one such novel transporter of the Monosaccharide Transporter Family, the closest phylogenetic homolog of which is the chloroplast-localized glucose transporter pGlcT and that we therefore term plastidic glucose transporter 2 (pGlcT2). We show, using gene-complemented glucose uptake deficiency of an Escherichia coli ptsG/manXYZ mutant strain and biochemical characterization, that this protein specifically facilitates glucose transport, whereas other sugars do not serve as substrates. In addition, we demonstrate pGlcT2-GFP localized to the chloroplast envelope and that pGlcT2 is mainly produced in seedlings and in the rosette center of mature Arabidopsis plants. Therefore, in conjunction with molecular and metabolic data, we propose pGlcT2 acts as a glucose importer that can limit cytosolic glucose availability in developing pGlcT2-overexpressing seedlings. Finally, we show both overexpression and deletion of pGlcT2 resulted in impaired growth efficiency under long day and continuous light conditions, suggesting pGlcT2 contributes to a release of glucose derived from starch mobilization late in the light phase. Together, these data indicate the facilitator pGlcT2 changes the direction in which it transports glucose during plant development and suggest the activity of pGlcT2 must be controlled spatially and temporarily in order to prevent developmental defects during adaptation to periods of extended light.
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2013-02-27 | GSE39445 | GEO
Project description:Upon illumination, etiolated seedlings experience a transition from heterotrophic to photoautotrophic growth. During this process, the tetrapyrrole biosynthesis pathway provides chlorophyll for photosynthesis. This pathway has to be tightly controlled to prevent the accumulation of photoreactive metabolites and to provide stoichiometric amounts of chlorophyll for its incorporation into photosynthetic protein complexes. Therefore, plants have evolved regulatory mechanisms to synchronize the biosynthesis of chlorophyll and chlorophyll-binding proteins. Two phytochrome-interacting factors (PIF1 and PIF3) and the DELLA proteins, which are controlled by the gibberellin pathway, are key regulators of this process. Here, we show that impairment of TARGET OF RAPAMYCIN (TOR) activity in Arabidopsis (Arabidopsis thaliana), either by mutation of the TOR complex component RAPTOR1B or by treatment with TOR inhibitors, leads to a significantly reduced accumulation of the photoreactive chlorophyll precursor protochlorophyllide in darkness but an increased greening rate of etiolated seedlings after exposure to light. Detailed profiling of metabolic, transcriptomic, and physiological parameters revealed that the TOR-repressed lines not only grow slower, they grow in a nutrient-saving mode, which allows them to resist longer periods of low nutrient availability. Our results also indicated that RAPTOR1B acts upstream of the gibberellin-DELLA pathway and its mutation complements the repressed greening phenotype of pif1 and pif3 after etiolation.
2018-07-17 | GSE114639 | GEO