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首页> 外文期刊>Protoplasma: An International Journal of Cell Biology >ACTIN-MICROTUBULE INTERACTIONS IN THE ALGA NITELLA - ANALYSIS OF THE MECHANISM BY WHICH MICROTUBULE DEPOLYMERIZATION POTENTIATES CYTOCHALASINS EFFECTS ON STREAMING
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ACTIN-MICROTUBULE INTERACTIONS IN THE ALGA NITELLA - ANALYSIS OF THE MECHANISM BY WHICH MICROTUBULE DEPOLYMERIZATION POTENTIATES CYTOCHALASINS EFFECTS ON STREAMING

机译:藻类中的Actin-微管相互作用-微管解聚电位对细胞松弛素的作用机理分析

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摘要

In the characean alga Nitella, depolymerization of microtubules potentiates the inhibitory effects of cytochalasins on cytoplasmic streaming. Microtubule depolymerization lowers the cytochalasin B and D concentrations required to inhibit streaming, accelerates inhibition and delays streaming recovery. Because microtubule depolymerization does nor significantly alter H-3-cytochalasin B uptake and release, elevated intracellular cytochalasin concentrations are not the basis for potentiation. Instead, microtubule depolymerization causes actin to become more sensitive to cytochalasin. This increased sensitivity of actin is unlikely to be due to direct stabilization of actin by microtubules, however, because very few microtubules colocalize with the subcortical actin bundles that generate streaming. Furthermore, microtubule reassembly, but nor recovery of former transverse alignment, is sufficient for restoring the normal cellular responses to cytochalasin D. We hypothesize that either tubulin or microtubule-associated proteins, released when microtubules depolymerize, interact with the actin cytoskeleton and sensitize it to cytochalasin. [References: 43]
机译:在沙棘藻Nitella中,微管的解聚作用增强了细胞松弛素对细胞质流的抑制作用。微管解聚降低了抑制细胞流动所需的细胞松弛素B和D的浓度,加速了抑制作用并延迟了细胞流动的恢复。由于微管解聚也不会显着改变H-3-cytochalasin B的摄取和释放,因此升高的细胞内细胞松弛素浓度不是增强的基础。相反,微管解聚导致肌动蛋白对细胞松弛素变得更加敏感。肌动蛋白的这种增加的敏感性不太可能是由于微管对肌动蛋白的直接稳定作用,但是,因为很少有微管与产生流的皮层下肌动蛋白束共定位。此外,微管重组,但也不能恢复以前的横向排列,足以恢复对细胞松弛素D的正常细胞反应。我们假设微管解聚时释放的微管蛋白或微管相关蛋白会与肌动蛋白细胞骨架相互作用并使之敏感。细胞松弛素。 [参考:43]

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