Yamada Y, Okamoto K
Department of Botany, Faculty of Science, Kyoto University, Japan.
Dev Biol. 1994 Jan;161(1):296-301. doi: 10.1006/dbio.1994.1029.
The prestalk-specific genes ecmA and ecmB in Dictyostelium are both induced by cAMP and DIF-1. In an attempt to understand the control mechanism of the differential expression of the two genes in multicellular aggregates, we examined the requirement for additional cellular interaction using low-cell-density cultures. We show that the whole process of inducing expression of these genes depends on high cell density. However, cells which have become responsive to DIF-1 expressed both genes at a low cell density in the presence of DIF-1 when incubated in a medium previously conditioned by developing cells. 8-Br-cAMP, which is believed to penetrate the cell membrane and activate protein kinase A, induced ecmB, but not ecmA, in the absence of the conditioned medium. These results suggest that there may be a specific inducer of ecmB in the conditioned medium which acts via activation of protein kinase A. Previously, the two genes were shown to respond differently to cAMP in late development at high cell densities, where there were cellular interactions. However, cAMP given to low-density-plated cells inhibited the conditioned medium-dependent induction of both genes to the same extent, suggesting that cAMP itself does not directly show the different effects on the two genes.
盘基网柄菌中前柄特异性基因ecmA和ecmB均由cAMP和DIF-1诱导。为了理解这两个基因在多细胞聚集体中差异表达的调控机制，我们使用低细胞密度培养来研究额外细胞相互作用的必要性。我们发现这些基因诱导表达的整个过程依赖于高细胞密度。然而，在先前由发育中的细胞预处理过的培养基中培养时，对DIF-1有反应的细胞在低细胞密度且存在DIF-1的情况下会表达这两个基因。据信能穿透细胞膜并激活蛋白激酶A的8-溴-cAMP，在没有预处理培养基的情况下可诱导ecmB，但不能诱导ecmA。这些结果表明，预处理培养基中可能存在一种通过激活蛋白激酶A起作用的ecmB特异性诱导物。此前研究表明，在高细胞密度的后期发育阶段，存在细胞相互作用时，这两个基因对cAMP的反应不同。然而，给予低密度平板培养细胞的cAMP会同等程度地抑制这两个基因的预处理培养基依赖性诱导，这表明cAMP本身并不会直接对这两个基因产生不同影响。
