Shinnick T M, Lerner R A
Proc Natl Acad Sci U S A. 1980 Aug;77(8):4788-92. doi: 10.1073/pnas.77.8.4788.
The loss of the lectin-like activity of a 26,000-dalton carbohydrate-binding protein (CBP-26) results in the loss of aggregation competence and cell-cell cohesiveness in developing cells of Dictyostelium discoideum. The lesion responsible for this phenotype behaves like a mutation in the structural gene for CBP-26, maps in linkage group II, and has been designated cbpA1. In aggregation-competent revertants, the degree of aggregation competence and cell-cell cohesiveness is directly related to the specific activity of CBP-26. Thus, CBP-26 appears to play an essential role in cell aggregation through the cell-cell cohesion process.
26000道尔顿的碳水化合物结合蛋白(CBP - 26)的凝集素样活性丧失,导致盘基网柄菌发育细胞中聚集能力和细胞间黏附性的丧失。导致这种表型的损伤表现得就像CBP - 26结构基因中的一个突变,定位于连锁群II,已被命名为cbpA1。在具有聚集能力的回复突变体中,聚集能力和细胞间黏附性的程度与CBP - 26的比活性直接相关。因此,CBP - 26似乎通过细胞间黏附过程在细胞聚集中发挥重要作用。