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肌球蛋白ATP酶抑制剂2,3-丁二酮-2-一肟(BDM)可抑制裂殖酵母粟酒裂殖酵母中的顶端生长和胞质分裂。

The myosin ATPase inhibitor 2,3-butanedione-2-monoxime (BDM) inhibits tip growth and cytokinesis in the fission yeast, Schizosaccharomyces pombe.

作者信息

May K M, Wheatley S P, Amin V, Hyams J S

机构信息

Department of Biology, University College London, UK.

出版信息

Cell Motil Cytoskeleton. 1998;41(2):117-25. doi: 10.1002/(SICI)1097-0169(1998)41:2<117::AID-CM3>3.0.CO;2-B.

Abstract

The growth of fission yeast cultures was reversibly inhibited by exposure to the myosin-ATPase inhibitor 2,3-butanedione-2-monoxime (BDM). Wild-type cells treated with 20 mM BDM for approximately two generation times were smaller than untreated controls and had a septation index approximately twice that seen in the absence of the inhibitor. The organization of actin at the cell poles was somewhat disorganized in the presence of BDM; however, cells formed a cytokinetic actin ring. When nitrogen-starved stationary-phase cells were reinoculated into fresh medium in the presence of BDM, the time taken to repolarize the actin cytoskeleton and to resume the characteristic vegetative cell shape before initiation of the first cell division were both substantially delayed. BDM significantly inhibited the increase in cell length of cdc25.22 cells arrested for cell cycle progress by incubation at the restrictive temperature and substantially delayed the initiation of both mitosis and cytokinesis in arrested cdc25.22 cells after release of the temperature block. These results suggest that tip growth and cytokinesis--processes in fission yeast that involve the actin cytoskeleton--also require myosin activity.

摘要

裂殖酵母培养物的生长可通过暴露于肌球蛋白 - ATP酶抑制剂丁二酮 - 2 - 单肟(BDM)而被可逆性抑制。用20 mM BDM处理约两个世代时间的野生型细胞比未处理的对照细胞小,其隔膜指数约为不存在抑制剂时的两倍。在BDM存在的情况下,细胞极处肌动蛋白的组织有些紊乱;然而,细胞形成了细胞分裂肌动蛋白环。当在BDM存在的情况下将氮饥饿的静止期细胞重新接种到新鲜培养基中时,肌动蛋白细胞骨架重新极化以及在第一次细胞分裂开始前恢复典型的营养细胞形状所需的时间都被显著延迟。BDM显著抑制了因在限制温度下孵育而停滞于细胞周期进程的cdc25.22细胞的细胞长度增加,并在温度阻断解除后,显著延迟了停滞的cdc25.22细胞中 mitosis 和细胞分裂的起始。这些结果表明,裂殖酵母中涉及肌动蛋白细胞骨架的顶端生长和细胞分裂过程也需要肌球蛋白活性。

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