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首页> 外文期刊>Cell structure and function >Expression of a 66-kD Heat Shock Protein Associated with the Process of Cyst Formation of a True Slime Mold, Physarum polycephalum.
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Expression of a 66-kD Heat Shock Protein Associated with the Process of Cyst Formation of a True Slime Mold, Physarum polycephalum.

机译:66-kD热激蛋白的表达与真正的粘液霉菌多头poly的囊肿形成过程有关。

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References(28) Cited-By(17) Under unfavorable conditions for growth, haploid myxoamoebae of Physarum polycephalum retracted their pseudopodia and changed their cell shape into disk-like form, after which they constructed the cell walls to form microcysts. These morphological changes of haploid cells were associated with changes in intracellular distribution of actin filaments. Staining with phalloidin showed that actin filaments were almost uniformly distributed throughout the cytoplasm of the myxoamoebae. Whenthese cells were transferred to a cyst-inducing medium, the actin structures changed into short rods or dots, after which the rods/dots disappeared in the microcysts. Anincubation of the myxoamoebaein the cyst-inducing medium caused the synthesis of several proteins, among which a 66-kD protein was most prominently induced. The morphological changes and the induction of the 66-kD protein was pronounced at elevated temperatures, e.g. 40°C. The 66-kD protein was not induced, however, when plasmodia of the same species were incubated at 40°C. W efound that the 66- kD protein was co-precipitated with polymerized actin and bound to ATP-agarose. A double staining of the disk-shaped cells with anti-66-kD protein antibody and phalloidin revealed superimposable localization of the 66-kD protein and actin filaments in the short rods or dots. Although the induction of the 66-kD protein was enhanced at high temperatures, the protein was immunologically unrelated to the common heat shock proteins, HSP70 and HSP90, those are highly conserved during evolution. These results indicate that the 66-kD protein is a novel heat shock protein which is specifically expressed during cyst formation.
机译:参考文献(28)被引用并(17)在不利的生长条件下,poly头的单倍体粘线虫撤回了伪足并将其细胞形状改变为圆盘状,然后它们构建了细胞壁以形成微囊。单倍体细胞的这些形态变化与肌动蛋白丝的胞内分布变化有关。用鬼笔环肽染色表明,肌动蛋白丝几乎均匀地分布在黏附阿米巴的整个细胞质中。当这些细胞转移到囊肿诱导培养基中时,肌动蛋白的结构变成短杆或点,此后杆/点在微囊中消失。在囊肿诱导培养基中对粘氨阿布酸的孵育导致了几种蛋白质的合成,其中最突出地诱导了66 kD蛋白质。 66-kD蛋白的形态变化和诱导在升高的温度下,例如在室温下显着。 40℃。但是,当相同物种的质膜在40°C下孵育时,不会诱导66-kD蛋白。我们发现66 kD蛋白与聚合的肌动蛋白共沉淀并与ATP-琼脂糖结合。用抗66-kD蛋白抗体和鬼笔环肽对圆盘状细胞进行双重染色,发现66-kD蛋白和肌动蛋白丝在短杆或圆点中重叠存在。尽管在高温下增强了66 kD蛋白的诱导,但该蛋白在免疫学上与常见的热激蛋白HSP70和HSP90无关,它们在进化过程中高度保守。这些结果表明66-kD蛋白是在囊肿形成过程中特异性表达的新型热激蛋白。

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