Kesbeke F, Van Haastert P J
Zoological Laboratory, University of Leiden, The Netherlands.
Dev Biol. 1988 Dec;130(2):464-70. doi: 10.1016/0012-1606(88)90342-9.
Extracellular cAMP induces the intracellular synthesis and subsequent secretion of cAMP in Dictyostelium discoideum (relay). cAMP relay was strongly diminished in mutant HB3 which shows abnormal development by making very small fruiting bodies. Extracellular cAMP binds to receptors on the surface of mutant cells and induces the rapid activation of adenylate cyclase. Intracellular cAMP rises to a concentration as high as that in wild-type cells but only a very small amount of cAMP is secreted. cAMP secretion in wild-type cells starts immediately after cAMP production, and is proportional to the intracellular cAMP concentration. In the mutant cells cAMP secretion starts a few minutes after cAMP production; by that time most of the intracellular cAMP is already degraded by phosphodiesterase and little cAMP is available for secretion. We conclude that mutant HB3 has a defect in the mechanism by which Dictyostelium cells secrete cAMP.
细胞外的环磷酸腺苷(cAMP)可诱导盘基网柄菌细胞内合成cAMP并随后分泌cAMP(信号中继)。在突变体HB3中,cAMP信号中继显著减弱,该突变体通过形成非常小的子实体而表现出异常发育。细胞外的cAMP与突变体细胞表面的受体结合,并诱导腺苷酸环化酶的快速激活。细胞内的cAMP浓度升高至与野生型细胞中一样高的水平,但仅分泌出非常少量的cAMP。野生型细胞中的cAMP分泌在cAMP产生后立即开始,并且与细胞内cAMP浓度成正比。在突变体细胞中,cAMP分泌在cAMP产生几分钟后开始;到那时,大多数细胞内的cAMP已经被磷酸二酯酶降解,几乎没有cAMP可用于分泌。我们得出结论,突变体HB3在盘基网柄菌细胞分泌cAMP的机制中存在缺陷。