...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Molecular biology of the cell >Direct evidence for a critical role of myosin II in budding yeast cytokinesis and the evolvability of new cytokinetic mechanisms in the absence of myosin II
【24h】

Direct evidence for a critical role of myosin II in budding yeast cytokinesis and the evolvability of new cytokinetic mechanisms in the absence of myosin II

机译：在没有肌球蛋白II的情况下，肌球蛋白II在发芽酵母胞质分裂中的关键作用和新细胞动力学机制的演变的直接证据

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

In the budding yeast Saccharomyces cerevisiae, an actomyosin-based contractile ring is present during cytokinesis, as occurs in animal cells. However, the precise requirement for this structure during budding yeast cytokinesis has been controversial. Here we show that deletion of MYO1, the single myosin II gene, is lethal in a commonly used strain background. The terminal phenotype of myo1Delta is interconnected chains of cells, suggestive of a cytokinesis defect. To further investigate the role of Myo1p in cytokinesis, we conditionally disrupted Myo1 function by using either a dominant negative Myo1p construct or a strain where expression of Myo1p can be shut-off. Both ways of disruption of Myo1 function result in a failure in cytokinesis. Additionally, we show that a myo1Delta strain previously reported to grow nearly as well as the wild type contains a single genetic suppressor that alleviates the severe cytokinesis defects of myo1Delta. Using fluorescence time-lapse imaging and electron microscopy techniques, we show that cytokinesis in this strain is achieved through formation of multiple aberrant septa. Taken together, these results strongly suggest that the actomyosin ring is crucial for successful cytokinesis in budding yeast, but new cytokinetic mechanisms can evolve through genetic changes when myosin II function is impaired. [References: 42]
机译：在萌芽的酿酒酵母中，如在动物细胞中一样，在胞质分裂过程中存在基于肌动球蛋白的收缩环。但是，在发芽酵母胞质分裂过程中对该结构的确切要求一直存在争议。在这里，我们显示，MYO1（单个肌球蛋白II基因）的缺失在常用菌株背景中具有致命性。 myo1Delta的终端表型是相互连接的细胞链，提示胞质分裂缺陷。为了进一步研究Myo1p在胞质分裂中的作用，我们有条件地通过使用显性阴性Myo1p构建体或可以关闭Myo1p表达的菌株来破坏Myo1功能。两种破坏Myo1功能的方法都会导致胞质分裂失败。此外，我们显示，以前报道的myo1Delta菌株几乎与野生型一样生长，包含一个单一的基因抑制因子，可减轻myo1Delta的严重胞质分裂缺陷。使用荧光延时成像和电子显微镜技术，我们表明该菌株的胞质分裂是通过形成多个异常隔而实现的。综上所述，这些结果强烈表明，肌动球蛋白环对于发芽酵母中成功的胞质分裂是至关重要的，但是当肌球蛋白II功能受损时，新的细胞动力学机制可通过遗传改变而发展。 [参考：42]

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