Magdolen V, Drubin D G, Mages G, Bandlow W
Institut für Genetik und Mikrobiologie der Universität München, Germany.
FEBS Lett. 1993 Jan 18;316(1):41-7. doi: 10.1016/0014-5793(93)81733-g.
Overproduction of actin is lethal to yeast cells. In contrast, overexpression of the profilin gene, PFY1, encoding an actin-binding protein, leads to no very obvious phenotype. Interestingly, profilin overproduction can compensate for the deleterious effects of too much actin in a profilin concentration-dependent manner. Our results, thus, document that actin and profilin interact in vivo. Immunofluorescence studies suggest that suppression works by reducing actin assembly. We observed, however, that even massive overproduction of profilin fails to fully restore the wild-type phenotype (e.g. the wild-type appearance of the actin microfilament system). This may indicate that actin monomer sequestration is not the only mechanism by which the balance of actin polymerization is controlled.
肌动蛋白的过量产生对酵母细胞是致命的。相比之下，编码肌动蛋白结合蛋白的原肌球蛋白基因PFY1的过表达不会导致非常明显的表型。有趣的是，原肌球蛋白的过量产生可以以原肌球蛋白浓度依赖性方式补偿过多肌动蛋白的有害影响。因此，我们的结果证明肌动蛋白和原肌球蛋白在体内相互作用。免疫荧光研究表明，抑制作用是通过减少肌动蛋白组装来实现的。然而，我们观察到，即使原肌球蛋白大量过表达也无法完全恢复野生型表型（例如肌动蛋白微丝系统的野生型外观）。这可能表明肌动蛋白单体隔离不是控制肌动蛋白聚合平衡的唯一机制。
