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The modulation of leaf metabolism plays a role in salt tolerance of Cymodocea nodosa exposed to hypersaline stress in mesocosms

机译:叶片代谢的调节在中膜中暴露于高盐胁迫下的结节藻的耐盐性中起作用

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摘要

Applying proteomics, we tested the physiological responses of the euryhaline seagrassCymodocea nodosa to deliberate manipulation of salinity in a mesocosm system.Plants were subjected to a chronic hypersaline condition (43 psu) to compare proteinexpression and plant photochemistry responses after 15 and 30 days of exposurewith those of plants cultured under normal/ambient saline conditions (37 psu). Resultsshowed a general decline in the expression level of leaf proteins in hypersaline stressedplants, with more intense reductions after long-lasting exposure. Specifically, thecarbon-fixing enzyme RuBisCo displayed a lower accumulation level in stressed plantsrelative to controls. In contrast, the key enzymes involved in the regulation of glycolysis,cytosolic glyceraldehyde-3-phosphate dehydrogenase, enolase 2 and triose-phosphateisomerase, showed significantly higher accumulation levels. These responses suggesteda shift in carbon metabolism in stressed plants. Hypersaline stress also induced asignificant alteration of the photosynthetic physiology of C. nodosa by means of a downregulationin structural proteins and enzymes of both PSII and PSI. However we foundan over-expression of the cytochrome b559 alpha subunit of the PSII initial complex,which is a receptor for the PSII core proteins involved in biogenesis or repair processesand therefore potentially involved in the absence of effects at the photochemical levelof stressed plants. As expected hypersalinity also affects vacuolar metabolism byincreasing the leaf cell turgor pressure and enhancing the up-take of Na+ by overaccumulatingthe tonoplast specific intrinsic protein pyrophosphate-energized inorganicpyrophosphatase (H(+)-PPase) coupled to the Na+/H+-antiporter. The modulation ofcarbon metabolism and the enhancement of vacuole capacity in Na+ sequestration andosmolarity changes are discussed in relation to salt tolerance of C. nodosa.
机译:应用蛋白质组学方法,我们测试了欧洲淡水海草(Cymodocea nodosa)对中膜系统中盐度操纵的生理反应,将植物置于慢性高盐条件(43 psu)下,与暴露15和30天后比较蛋白质表达和植物光化学反应。在正常/环境盐水条件下(37 psu)培养的植物数量。结果表明,高盐胁迫植物的叶片蛋白表达水平普遍下降,长期暴露后下降幅度更大。具体而言,固碳酶RuBisCo相对于对照在胁迫植物中显示出较低的积累水平。相比之下,参与糖酵解调节的关键酶胞质甘油醛-3-磷酸脱氢酶,烯醇酶2和磷酸三糖磷酸异构酶则显示出明显更高的积累水平。这些反应表明胁迫植物的碳代谢发生了变化。高盐胁迫还通过下调PSII和PSI的结构蛋白和酶来诱导结节梭菌的光合生理发生显着变化。然而,我们发现了PSII初始复合物的细胞色素b559α亚基的过度表达,该复合物是参与生物发生或修复过程的PSII核心蛋白的受体,因此潜在地涉及在胁迫植物的光化学水平上没有影响。如预期的那样,高盐度还通过增加叶细胞膨大压力并通过过度积累与Na + / H +-反向偶联的液泡膜特异性内在蛋白焦磷酸盐激发的无机焦磷酸酶(H(+)-PPase)来增加液泡膨胀并增加Na +的吸收,从而影响液泡代谢。碳结节的耐盐性讨论了碳代谢的调节和液泡容量在Na +螯合和摩尔渗透压浓度变化中的增强。

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