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环磷酸腺苷诱导盘基网柄菌聚集后分化。细胞表面环磷酸腺苷受体参与的证据。

Induction of post-aggregative differentiation in Dictyostelium discoideum by cAMP. Evidence of involvement of the cell surface cAMP receptor.

作者信息

Schaap P, van Driel R V

出版信息

Exp Cell Res. 1985 Aug;159(2):388-98. doi: 10.1016/s0014-4827(85)80012-4.

Abstract

Exogenous cAMP is known to induce post-aggregative differentiation in Dictyostelium discoideum under conditions that normal development is blocked. We have analysed the cyclic nucleotide specificity, the effect of modulation of the cAMP signal and the dose-response relationship of the induction of two independent markers of post-aggregative differentiation, i.e., a prespore cell-specific antigen detected by a monoclonal antibody, and the activity of glycogen phosphorylase. Our results confirm that high concentrations of cAMP (10(-6)-10(-3)M) are required for the induction of these markers. The cells are shown not to adapt to the cAMP signal. The cyclic nucleotide specificity of induction agrees with the specificity of the cell surface cAMP receptor, but is very dissimilar to the specificity of the intracellular cAMP-dependent protein kinase. It is thus unlikely that cAMP leaks into the cell and activates the cAMP-dependent protein kinase directly. Instead, the induction of post-aggregative differentiation by cAMP seems to be mediated by cell surface cAMP receptors.

摘要

已知在正常发育受阻的条件下,外源性环磷酸腺苷(cAMP)可诱导盘基网柄菌进行聚集后分化。我们分析了环核苷酸特异性、cAMP信号调节的影响以及诱导聚集后分化的两个独立标志物(即通过单克隆抗体检测到的前孢子细胞特异性抗原和糖原磷酸化酶的活性)的剂量反应关系。我们的结果证实,诱导这些标志物需要高浓度的cAMP(10⁻⁶ - 10⁻³M)。结果表明细胞不会适应cAMP信号。诱导的环核苷酸特异性与细胞表面cAMP受体的特异性一致,但与细胞内cAMP依赖性蛋白激酶的特异性非常不同。因此,cAMP不太可能泄漏到细胞中并直接激活cAMP依赖性蛋白激酶。相反,cAMP诱导的聚集后分化似乎是由细胞表面cAMP受体介导的。

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