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      Low-cesium rice: mutation in OsSOS2 reduces radiocesium in rice grains

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          Abstract

          In Japan, radiocesium contamination in foods has become of great concern and it is a primary issue to reduce grain radiocesium concentration in rice ( Oryza sativa L.). Here, we report a low-cesium rice mutant 1 ( lcs1) with the radiocesium concentration in grain about half that in the wild-type cultivar. Genetic analyses revealed that a mutation in OsSOS2, which encodes a serine/threonine-protein kinase required for the salt overly sensitive (SOS) pathway in plants, is responsible for the decreased cesium (Cs) concentrations in lcs1. Physiological analyses showed that Cs + uptake by lcs1 roots was significantly decreased under low-potassium (K +) conditions in the presence of sodium (Na +) (low K +/Na +). The transcript levels of several K + and Na + transporter genes, such as OsHAK1, OsHAK5, OsAKT1, and OsHKT2;1 were significantly down-regulated in lcs1 grown at low K +/Na +. The decreased Cs + uptake in lcs1 might be closely related to the lower expression of these genes due to the K +/Na + imbalance in the lcs1 roots caused by the OsSOS2 mutation. Since the lcs1 plant had no significant negative effects on agronomic traits when grown in radiocesium-contaminated paddy fields, this mutant could be used directly in agriculture for reducing radiocesium in rice grains.

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          Most cited references45

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          A statistical framework for SNP calling, mutation discovery, association mapping and population genetical parameter estimation from sequencing data

          (2013)
          Motivation: Most existing methods for DNA sequence analysis rely on accurate sequences or genotypes. However, in applications of the next-generation sequencing (NGS), accurate genotypes may not be easily obtained (e.g. multi-sample low-coverage sequencing or somatic mutation discovery). These applications press for the development of new methods for analyzing sequence data with uncertainty. Results: We present a statistical framework for calling SNPs, discovering somatic mutations, inferring population genetical parameters and performing association tests directly based on sequencing data without explicit genotyping or linkage-based imputation. On real data, we demonstrate that our method achieves comparable accuracy to alternative methods for estimating site allele count, for inferring allele frequency spectrum and for association mapping. We also highlight the necessity of using symmetric datasets for finding somatic mutations and confirm that for discovering rare events, mismapping is frequently the leading source of errors. Availability: http://samtools.sourceforge.net. Contact: hengli@broadinstitute.org.
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            The Arabidopsis thaliana salt tolerance gene SOS1 encodes a putative Na+/H+ antiporter.

            In Arabidopsis thaliana, the SOS1 (Salt Overly Sensitive 1) locus is essential for Na(+) and K(+) homeostasis, and sos1 mutations render plants more sensitive to growth inhibition by high Na(+) and low K(+) environments. SOS1 is cloned and predicted to encode a 127-kDa protein with 12 transmembrane domains in the N-terminal part and a long hydrophilic cytoplasmic tail in the C-terminal part. The transmembrane region of SOS1 has significant sequence similarities to plasma membrane Na(+)/H(+) antiporters from bacteria and fungi. Sequence analysis of various sos1 mutant alleles reveals several residues and regions in the transmembrane as well as the tail parts that are critical for SOS1 function in plant salt tolerance. SOS1 gene expression in plants is up-regulated in response to NaCl stress. This up-regulation is abated in sos3 or sos2 mutant plants, suggesting that it is controlled by the SOS3/SOS2 regulatory pathway.
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              Regulation of SOS1, a plasma membrane Na+/H+ exchanger in Arabidopsis thaliana, by SOS2 and SOS3.

              Maintaining low levels of sodium ions in the cell cytosol is critical for plant growth and development. Biochemical studies suggest that Na(+)/H(+) exchangers in the plasma membrane of plant cells contribute to cellular sodium homeostasis by transporting sodium ions out of the cell; however, these exchangers have not been identified at the molecular level. Genetic analysis has linked components of the salt overly sensitive pathway (SOS1-3) to salt tolerance in Arabidopsis thaliana. The predicted SOS1 protein sequence and comparisons of sodium ion accumulation in wild-type and sos1 plants suggest that SOS1 is involved directly in the transport of sodium ions across the plasma membrane. To demonstrate the transport capability of SOS1, we studied Na(+)/H(+)-exchange activity in wild-type and sos plants using highly purified plasma membrane vesicles. The results showed that plasma membrane Na(+)/H(+)-exchange activity was present in wild-type plants treated with 250 mM NaCl, but this transport activity was reduced by 80% in similarly treated sos1 plants. In vitro addition of activated SOS2 protein (a protein kinase) increased Na(+)/H(+)-exchange activity in salt-treated wild-type plants 2-fold relative to transport without added protein. However, the addition of activated SOS2 did not have any stimulatory effect on the exchange activity in sos1 plants. Although vesicles of sos2 and sos3 plants had reduced plasma membrane Na(+)/H(+)-exchange activity, transport activity in both increased with the addition of activated SOS2 protein. These results demonstrate that SOS1 contributes to plasma membrane Na(+)/H(+) exchange and that SOS2 and SOS3 regulate SOS1 transport activity.
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                Author and article information

                Contributors
                isatoru@affrc.go.jp
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                25 May 2017
                25 May 2017
                2017
                : 7
                : 2432
                Affiliations
                [1 ]ISNI 0000 0001 2222 0432, GRID grid.416835.d, Institute for Agro-Environmental Sciences, , National Agriculture and Food Research Organization (NARO), ; Tsukuba, 305-8604 Japan
                [2 ]ISNI 0000 0001 2222 0432, GRID grid.416835.d, Institute of Agrobiological Sciences, , NARO, ; Tsukuba, 305-8604 Japan
                [3 ]Hama Agricultural Regeneration Research Centre, Fukushima Agricultural Technology Centre, Minamisoma, 975-0007 Japan
                [4 ]Fruit Tree Research Centre, Fukushima Agricultural Technology Centre, Fukushima, 960-0231 Japan
                [5 ]ISNI 0000 0001 2222 0432, GRID grid.416835.d, Tohoku Agricultural Research Center, , NARO, ; Fukushima, 960-2156 Japan
                [6 ]ISNI 0000 0001 2222 0432, GRID grid.416835.d, Institute of Crop Science, , NARO, ; Tsukuba, 305-8518 Japan
                [7 ]ISNI 0000 0004 0376 441X, GRID grid.277489.7, , Iwate Biotechnology Research Center, ; Kitakami, 024-0003 Japan
                [8 ]GRID grid.410789.3, , Ishikawa Prefectural University, ; Ishikawa, 921-8836 Japan
                Article
                2243
                10.1038/s41598-017-02243-9
                5445092
                28546542
                83eb95af-f9b2-4a55-8b74-78557ff46593
                © The Author(s) 2017

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 12 October 2016
                : 10 April 2017
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