Molecular Mechanisms of Adhesion in Dictyostelium

组织内细胞的粘附是所有多细胞生物共同的基本细胞过程。卢米斯博士的研究重点是盘基骨鞘细胞黏附的机制，这种机制在聚集和随后的形态发生过程中发挥作用。他已经证明了一种表面糖蛋白gp24是在发育的最初几个小时内合成的。gp24特异性抗体在此期间阻断粘附，这种活性可以被高度纯化的gp24中和。编码gp24基因的克隆蛋白被连接到下游的肌动蛋白启动子上，从而产生反义RNA。在用该载体转化的细胞中，gp24的合成和细胞粘附的获得都延迟了约4小时。Loomis博士建议在野生型菌株和特别缺乏第二粘附机制（接触位点A）的菌株中通过基因替换来删除编码gp24的基因对。在整个发育过程中完全缺乏gp24的后果将完全取决于形态发生和随后的发育基因表达。在聚集之后，孢子前细胞中出现了另一种粘附机制，可以通过特异性抗血清的粘附阻断活性与前两种机制区分开来。Loomis博士建议充分描述第三种粘附机制的基本组成部分。

Adhesion of cells within tissues is a basic cellular process that is common to all multicellular organisms. Dr. Loomis is focusing his attention on the mechanisms of cell-cell adhesion in Dictyostelium that function during aggregation and subsequent morphogenesis. He has shown that a surface glycoprotein, gp24, is synthesized during the first few hours of development. Antibodies specific to gp24 block adhesion during this period and this activity can be neutralized by highly purified gp24. A cloned protein of the gene coding for gp24 was ligated downstream to an actin promoter such that antisense RNA would be generated. Both synthesis of gp24 and the acquisition of cell-cell adhesion is delayed about four hours in cell transformed with this vector. Dr. Loomis proposes to delete the pair of genes coding for gp24 by gene replacement in both wild type strains and in strains specifically lacking the second adhesion mechanism (contact sites A). The consequences of a complete lack of gp24 throughout development will be fully determined with respect to morphogenesis and subsequent developmental gene expression. Following aggregation another adhesion mechanism appears in prespore cells that can be distinguished from the first two mechanisms by the adhesion blocking activity of specific antisera. Dr. Loomis proposes to fully characterize the essential component(s) of the third adhesion mechanism.