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外向整流钾离子通道活性调节烟草BY-2细胞的细胞伸长和细胞分裂。

Outward-rectifying K+ channel activities regulate cell elongation and cell division of tobacco BY-2 cells.

作者信息

Sano Toshio, Kutsuna Natsumaro, Becker Dirk, Hedrich Rainer, Hasezawa Seiichiro

机构信息

Graduate School of Frontier Sciences, The University of Tokyo, Kashiwa, Chiba, Japan.

出版信息

Plant J. 2009 Jan;57(1):55-64. doi: 10.1111/j.1365-313X.2008.03672.x. Epub 2008 Oct 4.

DOI:10.1111/j.1365-313X.2008.03672.x
PMID:18778403
Abstract

Potassium ions (K+) are required for plant growth and development, including cell division and cell elongation/expansion, which are mediated by the K+ transport system. In this study, we investigated the role of K+ in cell division using tobacco BY-2 protoplast cultures. Gene expression analysis revealed induction of the Shaker-like outward K+ channel gene, NTORK1, under cell-division conditions, whereas the inward K+ channel genes NKT1 and NtKC1 were induced under both cell-elongation and cell-division conditions. Repression of NTORK1 gene expression by expression of its antisense construct repressed cell division but accelerated cell elongation even under conditions promoting cell division. A decrease in the K+ content of cells and cellular osmotic pressure in dividing cells suggested that an increase in cell osmotic pressure by K+ uptake is not required for cell division. In contrast, K+ depletion, which reduced cell-division activity, decreased cytoplasmic pH as monitored using a fluorescent pH indicator, SNARF-1. Application of K+ or the cytoplasmic alkalizing reagent (NH(4))(2)SO(4) increased cytoplasmic pH and suppressed the reduction in cell-division activity. These results suggest that the K+ taken up into cells is used to regulate cytoplasmic pH during cell division.

摘要

钾离子(K+)对于植物生长发育至关重要,包括细胞分裂以及由K+转运系统介导的细胞伸长/扩展。在本研究中,我们利用烟草BY-2原生质体培养来探究K+在细胞分裂中的作用。基因表达分析显示,在细胞分裂条件下,类Shaker外向K+通道基因NTORK1被诱导表达,而内向K+通道基因NKT1和NtKC1在细胞伸长和细胞分裂条件下均被诱导表达。通过表达其反义构建体来抑制NTORK1基因表达,即使在促进细胞分裂的条件下,也会抑制细胞分裂但加速细胞伸长。分裂细胞中K+含量和细胞渗透压的降低表明,细胞分裂并不需要通过摄取K+来增加细胞渗透压。相反,K+耗竭降低了细胞分裂活性,使用荧光pH指示剂SNARF-1监测发现细胞质pH下降。施加K+或细胞质碱化试剂(NH4)2SO4可提高细胞质pH并抑制细胞分裂活性的降低。这些结果表明,细胞摄取的K+用于在细胞分裂过程中调节细胞质pH。

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