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Ultrastructure of Sweet Orange Ripening Fruit (Citrus sinensis L.Osbeck) and the Role of Hydrolases in Dietary Fiber Degradation

机译:甜橙成熟果实柑桔的超微结构及其水解酶在膳食纤维降解中的作用

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Sweet orange (Citrus sinensis L. Osbeck) fruit is an important source of dietary fiber, which consists of a variety of non starch polysaccharides. The change of dietary fiber and polysaccharides leading to fruit softening is complex, which includes the coordinated and interdependent activities of a range of cell wall modifying proteins. Polygalacturonase (PG) activity is largely responsible for pectin depolymerization and solubilization, but PG-mediated pectin depolymerization requires pectin to be de-methylesterified by Pectinesterase (PE). All these pectinmodifying proteins affect the integrity of the middle lamella, which controls cell-to-cell adhesion and thus influences fruit texture. In contrast, the primary cell wall changes caused by the activities of β-galactosidase (β-Gal) and cellulase (Cx) early in ripening may restrict or control the activities of other ripening-related enzymes necessary for the fruit softening process. Taken together, we could consider that the changes of dietary fibre concentration and composition were caused by the solubilisation and depolymerisation of pectins in middle lamella and the disintegration of the primary cell wall. The data described above show that the disassembly of sweet orange fruit cell wall components during fruit ripening was brought about by a range of enzyme activities, and the presence of these mRNAs, and enzymic activities were in accordance with enzyme action in the living plant cell.
机译:甜橙(Citrus sinensis L. Osbeck)果实是膳食纤维的重要来源,其由多种非淀粉多糖组成。导致水果软化的膳食纤维和多糖的变化是复杂的,其中包括一系列细胞壁修饰蛋白的协同和相互依赖的活性。聚半乳糖醛酸酶(PG)的活性主要负责果胶的解聚和增溶作用,但是PG介导的果胶解聚需要果胶被果胶酯酶(PE)脱甲基化。所有这些果胶修饰蛋白都会影响中间层的完整性,从而控制细胞间的粘附,从而影响果实的质地。相反,在成熟早期,由β-半乳糖苷酶(β-Gal)和纤维素酶(Cx)的活性引起的原代细胞壁变化可能会限制或控制水果软化过程所必需的其他与成熟相关的酶的活性。两者合计,我们可以认为,膳食纤维浓度和组成的变化是由于果胶在中间层中的溶解和解聚以及原代细胞壁的分解引起的。上述数据表明,在果实成熟期间,甜橙果实细胞壁成分的分解是由一系列酶活性引起的,并且这些mRNA的存在和酶活性与活植物细胞中的酶活性一致。

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