Control of cAMP‐induced gene expression by divergent signal transduction pathways

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Abstract
A compilation of literature data and recent experiments led to the following conclusions regarding cyclic adenosine 3′:5′ monophosphate (cAMP) regulation of gene expression. Several classes of cAMP‐induced gene expression can be discriminated by sensitivity to stimulation kinetics. The aggregation‐related genes respond only to nanomolar cAMP pulses. The prestalk‐related genes respond both to nano‐molar pulses and persistent micromolar stimulation. The prespore specific genes respond only to persistent micromolar stimulation. The induction of the aggregation‐ and prestalk‐related genes by nanomolar cAMP pulses may share a common transduction pathway, which does not involve cAMP, while involvement of the inositol 1,4,5‐trisphosphate (IP3)/Ca2+ pathway is unlikely. Induction of the expression of prespore and prestalk‐related genes by micromolar cAMP stimuli utilizes divergent signal processing mechanisms. cAMP‐induced prespore gene expression does not involve cAMP and probably also not cyclic guanosine 3′.5′ monophosphate (cGMP) as intracellular intermediate. Involvement of cAMP‐induced phospholipase C (PLC) activation in this pathway is suggested by the observation that IP3 and 1,2‐diacylglycerol (DAG) can induce prespore gene expression, albeit in a somewhat indirect manner and by the observation that Li+ and Ca2+ antagonists inhibit prespore gene expression. Cyclic AMP induction of prestalk‐related gene expression is inhibited by IP3 and DAG and promoted by Li+, and is relatively insensitive to Ca2+ antagonists, which indicates that PLC activation does not mediate prestalk‐related gene expression. Neither prespore nor prestalk‐related gene expression utilizes the sustained cAMP‐induced pHi increase as intracellular intermediate.