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    Sultr4;1 mutant seeds of Arabidopsis have an enhanced sulphate content and modified proteome suggesting metabolic adaptations to altered sulphate compartmentalization

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    <p>Abstract</p> <p>Background</p> <p>Sulphur is an essential macronutrient needed for the synthesis of many cellular components. Sulphur containing amino acids and stress response-related compounds, such as glutathione, are derived from reduction of root-absorbed sulphate. Sulphate distribution in cell compartments necessitates specific transport systems. The low-affinity sulphate transporters SULTR4;1 and SULTR4;2 have been localized to the vacuolar membrane, where they may facilitate sulphate efflux from the vacuole.</p> <p>Results</p> <p>In the present study, we demonstrated that the <it>Sultr4;1 </it>gene is expressed in developing Arabidopsis seeds to a level over 10-fold higher than the <it>Sultr4;2 </it>gene. A characterization of dry mature seeds from a <it>Sultr4;1 </it>T-DNA mutant revealed a higher sulphate content, implying a function for this transporter in developing seeds. A fine dissection of the <it>Sultr4;1 </it>seed proteome identified 29 spots whose abundance varied compared to wild-type. Specific metabolic features characteristic of an adaptive response were revealed, such as an up-accumulation of various proteins involved in sugar metabolism and in detoxification processes.</p> <p>Conclusions</p> <p>This study revealed a role for SULTR4;1 in determining sulphate content of mature Arabidopsis seeds. Moreover, the adaptive response of <it>sultr4;1 </it>mutant seeds as revealed by proteomics suggests a function of SULTR4;1 in redox homeostasis, a mechanism that has to be tightly controlled during development of orthodox seeds.</p

    Regulation of Sulfate Uptake and Assimilation--the Same or Not the Same?

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    International audiencePlant take up the essential nutrient sulfur as sulfate from the soil, reduce it, and assimilate into bioorganic compounds, with cysteine being the first product. Both sulfate uptake and assimilation are highly regulated by the demand for the reduced sulfur, by availability of nutrients, and by environmental conditions. In the last decade, great progress has been achieved in dissecting the regulation of sulfur metabolism. Sulfate uptake and reduction of activated sulfate, adenosine 5'-phosphosulfate (APS), to sulfite by APS reductase appear to be the key regulatory steps. Here, we review the current knowledge on regulation of these processes, with special attention given to similarities and differences

    Root uptake regulation: a central process for NPS homeostasis in plants.

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    International audienceHomeostasis of nitrogen, phosphorus and sulfur in growing plants requires a sustained intake of these elements into root cells. Under most situations, the adjustment of root N, P or S acquisition to the nutrient demand of the plant is hampered by the limiting and fluctuating availability of these elements in the soil. To cope with this constraint, higher plants modulate their root uptake capacity to compensate for the changes in external concentrations of the N, P or S sources. This adaptive response relies on both physiological and morphological changes in the root system, triggered by nutrient-specific sensing and signalling pathways. The underlying molecular mechanisms now begin to be elucidated. Key root membrane transport proteins have been identified, as well as molecular regulators that control root uptake systems or root system architecture in response to N, P or S availability. Significant but yet poorly understood interactions with carbon or hormone signalling have been unravelled, opening new routes for integrating the mechanisms of nutrient homeostasis into the whole plant

    H(+) Cotransports in Corn Roots as Related to the Surface pH Shift Induced by Active H(+) Excretion

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    The surface pH shift induced by active H(+) excretion in corn (Zea mays L.) roots was estimated using acetic acid influx as a pH probe (H Sentenac, C Grignon 1987 Plant Physiol 84: 1367-1372). At constant bulk pH, buffering the medium strongly reduced the magnitude of the surface pH shift. This was used to study the effect of surface pH shift on H(+) cotransports. In the absence of buffers, the surface pH shift increased with the bulk pH. Buffers decreased (32)Pi influx and this effect was stronger at pH 7.2 than at pH 5.8, and stronger in the absence than in the presence of an inhibitor of the proton pump (vanadate). Buffers exerted a similar depressive and pH-dependent effect on net NO(3)(−) uptake. They hyperpolarized the cell membrane, and stimulated (86)Rb(+) influx, K(+):H(+) net exchange, and malate accumulation. These results are consistent with the hypothesis that H(+) accumulation at the cell surface is effective in driving H(+) reentry. We concluded that the surface pH shift due to proton pump activity is involved in the energetic coupling of H(+) cotransports
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