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衰老诱导的光合作用丧失增强了细胞壁β-葡萄糖苷酶活性。

Senescence-induced loss in photosynthesis enhances cell wall beta-glucosidase activity.

机构信息

Laboratory of Biochemistry and Biophysics, School of Life Sciences, Sambalpur University, Jyoti Vihar 768019, Orissa, India.

出版信息

Physiol Plant. 2010 Mar;138(3):346-55. doi: 10.1111/j.1399-3054.2009.01327.x. Epub 2009 Nov 10.

DOI:10.1111/j.1399-3054.2009.01327.x
PMID:20028477
Abstract

A link between senescence-induced decline in photosynthesis and activity of beta-glucosidase is examined in the leaves of Arabidopsis. The enzyme is purified and characterized. The molecular weight of the enzyme is 58 kDa. It shows maximum activity at pH 5.5 and at temperature of 50 degrees C. Photosynthetic measurements and activity of the enzyme are conducted at different developmental stages including senescence of leaves. Senescence causes a significant loss in total chlorophyll, stomatal conductance, rate of evaporation and in the ability of the leaves for carbon dioxide fixation. The process also brings about a decline in oxygen evolution, quantum yield of photosystem II (PS II) and quantum efficiency of PS II photochemistry of thylakoid membrane. The loss in photosynthesis is accompanied by a significant increase in the activity of the cell wall-bound beta-glucosidase that breaks down polysaccharides to soluble sugars. The loss in photosynthesis as a signal for the enhancement in the activity of the enzyme is confirmed from the observation that incubation of excised mature leaves in continuous dark or in light with a photosynthesis inhibitor 3-(3,4-dichlorophenyl)-1, 1-dimethylurea (DCMU) that leads to sugar starvation enhances the activity of the enzyme. The work suggests that in the background of photosynthetic decline, the polysaccharides bound to cell wall that remains intact even during late phase of senescence may be the last target of senescing leaves for a possible source of sugar for remobilization and completion of the energy-dependent senescence program.

摘要

衰老诱导的光合作用下降与β-葡萄糖苷酶活性之间的联系在拟南芥叶片中进行了研究。该酶被纯化并进行了特性鉴定。酶的分子量为 58kDa。它在 pH5.5 和 50°C 的温度下显示出最大的活性。在不同的发育阶段(包括叶片衰老)进行光合作用测量和酶活性测定。衰老会导致总叶绿素、气孔导度、蒸发率和叶片固定二氧化碳的能力显著下降。该过程还导致氧释放、光系统 II(PS II)量子产量和类囊体膜 PS II 光化学的量子效率下降。光合作用的损失伴随着细胞壁结合的β-葡萄糖苷酶活性的显著增加,该酶将多糖分解为可溶性糖。从以下观察结果可以证实,光合作用的损失是作为增强酶活性的信号:将离体成熟叶片在连续黑暗或光合作用抑制剂 3-(3,4-二氯苯基)-1,1-二甲基脲(DCMU)存在的光下孵育,导致糖饥饿,从而增强了酶的活性。该研究表明,在光合作用下降的背景下,即使在衰老后期仍保持完整的细胞壁结合的多糖可能是衰老叶片的最后目标,可能是为了糖的再动员和完成依赖能量的衰老程序提供可能的来源。

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