Loss of tonoplast integrity programmed in tracheary element differentiation

Loss of tonoplast integrity programmed in tracheary element differentiation
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DOI:
10.1104/pp.121.3.763
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发表时间:
1999-11-01
期刊:
影响因子:
7.4
通讯作者:
Kuriyama, H
Kuriyama, H
中科院分区:
生物学1区
文献类型:
--
作者:
Kuriyama, H

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导管分子(TE)是维管植物发育过程中经历程序性细胞死亡的细胞类型的典型例子。液泡膜选择性透性的丧失,对应于液泡膜的解体,发生在细胞开始次生壁增厚之后,在百日菊(Zinnia elegans L.)细胞培养寻找与TE液泡特别相关的事件为理解细胞死亡机制提供了重要线索。运输荧光素,荧光有机阴离子,整个液泡膜急剧下降,在分化TE。液泡积累探针的能力也受到损害。丙磺舒,有机阴离子转运的抑制剂,治疗引起快速的细胞死亡的TE,并导致最终破坏的空泡,即使在其他类型的培养细胞。放线菌酮抑制了TE发展过程中液泡特性的这些变化。在TE分化诱导条件下培养的细胞中特异性mRNA积累被丙磺舒废除。这些结果表明,液泡膜通透性的变化促进了TE中的程序性细胞死亡。
A tracheary element (TE) is a typical example of a cell type that undergoes programmed cell death in the developmental processes of vascular plants. The loss of the selective permeability of the tonoplast, which corresponds to tonoplast disintegration, occurred after the cells commenced secondary wall thickening and played a pivotal role in the programmed cell death of TEs in a zinnia (Zinnia elegans L.) cell culture. A search for events specifically associated with the TE vacuole provided an important clue to the understanding of the cell death mechanism. The transport of fluorescein, a fluorescent organic anion, across the tonoplast declined drastically in differentiating TEs. The capacity of the vacuole to accumulate the probe was also impaired. Treatment with probenecid, an inhibitor of organic anion transport, caused rapid cell death of TEs and led to the ultimate disruption of the vacuole even in other types of cultured cells. These changes in vacuolar properties during TE development were suppressed by cycloheximide. Specific mRNA accumulation in cells cultured in a TE differentiation-inductive condition was abolished by probenecid. These results suggest that a change in vacuolar membrane permeability promotes programmed cell death in TEs.