CALCIUM-UPTAKE AND GP80 MESSENGER-RNA DESTABILIZATION FOLLOWS CAMP RECEPTOR DOWN-REGULATION IN DICTYOSTELIUM-DISCOIDEUM

The mechanism by which high concentrations of cAMP selectively destabi lize the gp80 mRNA in Dictyostelium discoideum was investigated. This treatment which leads to down-regulation of the cAMP receptor was also found to cause an increase in calcium uptake. Given this observation, we sought a role for calcium as a second messenger in the degradation of the gp80 mRNA. Changes in the mRNA levels were examined after trea ting cells with compounds known to alter their intracellular Ca2+ conc entrations. This included the use of A23187, Ca2+, 8-(N,N-diethylamino )octyl-3,4,5-trimethoxybenzoate HCl (TMB-8), LiCl and 8-p-chlorophenyl thioadenosine 3',5'-cyclic monophosphate (ClPhS-Ado-3':5'-P). The sum of the data suggest that it is the cAMP-induced influx of Ca2+ across the plasma membrane, as apposed to a cAMP-mediated release of Ca2+ fro m intracellular stores, that initiates gp80 mRNA degradation. Treatmen t of cells with Concanavalin A (ConA) to induce cAMP receptor down-reg ulation, also causes a reduction in gp80 mRNA levels and an increase i n calcium uptake.