Molecular genetic studies of sulfur nutrient response in Arabidopsis thaliana
Item
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Title
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Molecular genetic studies of sulfur nutrient response in Arabidopsis thaliana
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Identifier
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d_2009_2013:2cdf9191c102:11157
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identifier
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11551
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Creator
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Dan, Hanbin,
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Contributor
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Zhi-Liang Zheng
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Date
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2012
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Language
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English
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Publisher
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City University of New York.
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Subject
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Molecular biology | Plant sciences | Genetics | Arabidopsis thaliana | Genetic signaling | GFP | Map cloning | Sulfur
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Abstract
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The aim of this study was to isolate the components that are critical for the S nutrient response in plants. We used Arabidopsis thaliana as a model system. We first developed a S deficiency-responsive promoter:GUS reporter system. We confirmed that At2g44460 encoding a putative thioglucosidase exhibits the strongest induction by S deficiency. Interestingly, At2g44460 induction by S deficiency was suppressed by the application of auxin, a plant hormone. Together with other physiological and genetic evidence, we showed that auxin plays a negative regulatory role in S deficiency response. Furthermore, we found that S deficiency-induced expression of At2g44460 and a sulfate transporter gene (SULTR4;2) is dependent on the availability of C and N, which exhibit a synergistic interaction. Therefore, we designed a genetic screen by using the At2g44460 promoter:GUS reporter line (designated GHF1) with an aim of isolating the mutants that alter the expression of At2g44460 in response to C,N and S status.;Screen of the mutants resulted in the isolation of two allelic mutations on the SEL1 gene, which encodes a high-affinity transporter called SULTR1;2. SULTR1;2 is mainly responsible for transporting sulfate from the soil into the root. The two alleles, designated sel1-15 and sel1-16, have distinct missense mutations on the putative transmembrane domains, but they did not seem to cause mislocalization of the protein. As expected, these two mutations, like a SULTR1;2 null allele (sel1-10), abolish the sulfate uptake in both yeast and plant systems. They also reduced the accumulation of internal sulfate. However, a dose response study indicates that expression of the S deficiency-upregulated genes, At2g44460, SULTR4;2, LSU1 and SDI1, is higher in the mutants than that in WT under either the high sulfate treatment or under different sulfate treatments that result in similar levels of internal sulfate. Furthermore, these mutants reduced the sensitivity to external application of the high concentration of sulfate metabolites, suflite, Cys and GSH. Taken together, these results indicate that besides the sulfate transport function, SULTR1;2 likely acts as a sensor for S nutrient, adding this transporter to the growing list of nutrient transceptors.
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Type
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dissertation
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Source
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2009_2013.csv
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degree
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Ph.D.
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Program
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Biology
