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甜菜主根组织中蔗糖运输的膨压调节

Turgor regulation of sucrose transport in sugar beet taproot tissue.

作者信息

Wyse R E, Zamski E, Tomos A D

机构信息

United States Department of Agriculture, Agricultural Research Service, Utah State University, UMC 63, Logan, Utah 84322.

出版信息

Plant Physiol. 1986 Jun;81(2):478-81. doi: 10.1104/pp.81.2.478.

Abstract

Sink tissues that store osmotically active compounds must osmoregulate to prevent excessively high turgor. The ability to regulate turgor may be related to membrane transport of solutes and thus sink strength. To study this possibility, the kinetics of sugar uptake were determined in sugar beet (Beta vulgaris L.) taproot tissue discs over a range of cell turgors. Sucrose uptake followed biphasic kinetics with a high affinity saturating component below 20 millimolar and a low affinity linear component at higher concentrations. Glucose uptake exhibited only simple saturation type kinetics. The high affinity saturating component of sucrose and glucose uptake was inhibited by increasing cell turgor (decreasing external mannitol concentrations). The inhibition was evident as a decrease in V(max) but no effect on K(m). Sucrose uptake by tissue equilibrated in dilute buffer exhibited no saturating component. Ethylene glycol, a permeant osmoticum, had no effect on uptake kinetics, suggesting that the effect was due to changes in cell turgor and not due to decreased water potential per se. p-(Chloromercuri)benzene sulfonic acid (PCMBS) inhibited sucrose uptake at low but not high cell turgor. High cell turgor caused the tissue to become generally leaky to potassium, sucrose, amino acids, and reducing sugars. PCMBS had no effect on sucrose leakage, an indication that the turgor-induced leakage of sucrose was not via back flow through the carrier. The ability of the tissue to acidify the external media was turgor dependent with an optimum at 300 kilopascals. Acidification was sharply reduced at cell turgors above or below the optimum. The results suggest that the secondary transport of sucrose is reduced at high turgor as a result of inhibition of the plasma membrane ATPase. This inhibition of ATPase activity would explain the reduced V(max) and leakiness to low molecular weight solutes. Cell turgor is an important regulator of sucrose uptake in this tissue and thus may be an important determinant of sink strength in tissues that store sucrose.

摘要

储存渗透活性化合物的库组织必须进行渗透调节,以防止过高的膨压。调节膨压的能力可能与溶质的膜转运有关,进而与库强度相关。为了研究这种可能性,我们测定了甜菜(Beta vulgaris L.)主根组织圆盘在一系列细胞膨压下的糖分吸收动力学。蔗糖吸收遵循双相动力学,在20毫摩尔以下有一个高亲和力饱和成分,在较高浓度时有一个低亲和力线性成分。葡萄糖吸收仅表现出简单的饱和型动力学。蔗糖和葡萄糖吸收的高亲和力饱和成分会随着细胞膨压的增加(外部甘露醇浓度降低)而受到抑制。这种抑制表现为V(max)的降低,但对K(m)没有影响。在稀缓冲液中平衡的组织对蔗糖的吸收没有饱和成分。乙二醇,一种可渗透的渗透剂,对吸收动力学没有影响,这表明该效应是由于细胞膨压的变化,而不是由于水势本身的降低。对氯汞苯磺酸(PCMBS)在低细胞膨压下抑制蔗糖吸收,但在高细胞膨压下则不然。高细胞膨压导致组织对钾、蔗糖、氨基酸和还原糖普遍渗漏。PCMBS对蔗糖渗漏没有影响,这表明膨压诱导的蔗糖渗漏不是通过载体的反向流动。组织酸化外部介质的能力取决于膨压,在300千帕时有一个最佳值。在高于或低于最佳值的细胞膨压下,酸化会急剧降低。结果表明,在高膨压下,由于质膜ATP酶受到抑制,蔗糖的次级转运减少。这种ATP酶活性的抑制将解释V(max)的降低和对低分子量溶质的渗漏。细胞膨压是该组织中蔗糖吸收的重要调节因子,因此可能是储存蔗糖的组织中库强度的重要决定因素。

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