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首页> 外文期刊>Cell motility and the cytoskeleton >Chondramides, novel cyclodepsipeptides from myxobacteria, influence cell development and induce actin filament polymerization in the green alga Micrasterias.
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Chondramides, novel cyclodepsipeptides from myxobacteria, influence cell development and induce actin filament polymerization in the green alga Micrasterias.

机译:软骨素是一种来自粘细菌的新型环二肽,可影响细胞的发育并诱导绿藻微藻中的肌动蛋白丝聚合。

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摘要

The effects of chondramides A-D, new actin targeting cyclodepsipeptides from the myxobacterium Chondromyces crocatus, are probed on the unicellular green alga Micrasterias denticulata, a model organism for studies on cytomorphogenesis. All four chondramides readily enter the cells and cause severe shape malformations when applied during growth. However, the four derivatives have different lowest effective concentrations. Chondramide A: 20 microM, chondramide B: 15 microM, chondramide C: 5 microM chondramide D: 10 microM. At the ultrastructural level, chondramide C, the most effective drug, causes the appearance of abnormal, dense F-actin bundles, and a substantial increase in ER, which covers large parts of the developing semicell. Also the secondary cell wall is malformed by the drug. When chondramide C effects are investigated by means of indirect immunofluorescence, alterations of the F-actin system are also visible. Instead of the cortical F-actin network of untreated controls, distinct parts of the cell are covered by abundant F-actin aggregations. Phalloidin staining of chondramide C treated cells results in a decreased fluorescence in a time-dependent manner due to binding competitions between these drugs. F-actin polymerizing and bundling capacities of chondramides A-D are presented in Micrasterias for the first time, and may in future make this substances a useful tool for cell biological research. Copyright 2001 Wiley-Liss, Inc.
机译:在单细胞绿藻牙垢小,(Micrasterias denticulata)(一种用于细胞形态发生研究的模型生物)上探查了软骨粘液A-D(新的肌动蛋白靶向来自粘多糖的Chondromyces crocatus的环二肽)的作用。当在生长过程中使用时,所有四种软骨都容易进入细胞并引起严重的畸形。但是,这四种衍生物具有不同的最低有效浓度。软骨酰胺A:20 microM,软骨酰胺B:15 microM,软骨酰胺C:5 microM软骨酰胺D:10 microM。在超微结构水平上,最有效的药物软骨酰胺C导致出现异常的致密F-肌动蛋白束,并显着增加ER,从而覆盖了发育中的半细胞的大部分。辅助细胞壁也被药物畸形。当通过间接免疫荧光研究软骨酰胺C的作用时,F-肌动蛋白系统的改变也是可见的。代替未经处理的对照的皮质F-肌动蛋白网络,细胞的不同部分被丰富的F-肌动蛋白聚集所覆盖。由于这些药物之间的结合竞争,软骨酰胺C处理的细胞的鬼笔环肽染色会导致荧光减弱,并呈时间依赖性。软骨素A-D的F-肌动蛋白聚合和成束能力首次在微囊藻中出现,并且将来可能使这种物质成为细胞生物学研究的有用工具。版权所有2001 Wiley-Liss,Inc.

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