...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Protoplasma: An International Journal of Cell Biology >Inhibitors of myosin, but not actin, alter transport through Tradescantia plasmodesmata
【24h】

Inhibitors of myosin, but not actin, alter transport through Tradescantia plasmodesmata

机译：肌球蛋白的抑制剂，而不是肌动蛋白，改变通过Trade虫的运输

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Actin and myosin are components of plasmodesmata, the cytoplasmic channels between plant cells, but their role in regulating these channels is unclear. Here, we investigated the role of myosin in regulating plasmodesmata in a well-studied, simple system comprising single filaments of cells which form stamen hairs in Tradescantia virginiana flowers. Effects of myosin inhibitors were assessed by analysing cell-to-cell movement of fluorescent tracers microinjected into treated cells. Incubation in the myosin inhibitor, 2,3-butanedione monoxime (BDM) or injection of anti-myosin antibodies increased cell-cell transport of fluorescent dextrans, while treatment with the myosin inhibitor N-ethylmaleimide (NEM) decreased cell-cell transport. Pretreatment with the callose synthesis inhibitor, deoxy-d-glucose (DDG), enhanced transport induced by BDM treatment or injection of myosin antibodies but did not relieve NEM-induced reduction in transport. In contrast to the myosin inhibitors, cell-to-cell transport was unaffected by treatment with the actin polymerisation inhibitor, latrunculin B, after controlling for callose synthesis with DDG. Transport was increased following azide treatment, and reduced after injection of ATP, as in previous studies. We propose that myosin detachment from actin, induced by BDM, opens T. virginiana plasmodesmata whereas the firm attachment of myosin to actin, promoted by NEM, closes them.
机译：肌动蛋白和肌球蛋白是纤毛虫的成分，纤毛虫是植物细胞之间的细胞质通道，但是它们在调节这些通道中的作用尚不清楚。在这里，我们研究了肌球蛋白在调控细纤维瘤中的作用，该研究是在经过精心研究的简单系统中进行的，该系统包含单细丝细胞，这些细丝在紫露草花中形成雄蕊毛。通过分析显微注射到处理过的细胞中的荧光示踪剂，评估肌球蛋白抑制剂的作用。肌球蛋白抑制剂，2,3-丁二酮单肟（BDM）的孵育或抗肌球蛋白抗体的注射增加了荧光葡聚糖的细胞迁移，而肌球蛋白抑制剂N-乙基马来酰亚胺（NEM）处理则降低了细胞迁移。用call糖合成抑制剂，脱氧-d-葡萄糖（DDG）进行预处理，可以增强BDM处理或注射肌球蛋白抗体诱导的转运，但不能缓解NEM诱导的转运减少。与肌球蛋白抑制剂相反，在用DDG控制call合成后，肌动蛋白聚合抑制剂latrunculin B处理不会影响细胞间的转运。如先前的研究，叠氮化物处理后转运增加，而ATP注射后转运减少。我们建议肌动蛋白的肌动蛋白脱离，由BDM诱导，打开了T. virginiana plasmodesmata，而肌动蛋白对肌动蛋白的牢固附着（由NEM推动）将其关闭。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号