Progressive cytoplasmic tail truncations of the lutropin-choriogonadotropin receptor prevent agonist- or phorbol ester-induced phosphorylation, impair agonist- or phorbol ester-induced desensitization, and enhance agonist-induced receptor down-regulation.

Stably transfected human kidney 293 cells expressing the wild type rat LH/CG receptor (rLHR) or receptors with C-terminal tails truncated at residues 653, 631, or 628 (designated rLHR-t653, rLHR-t631, and rLHR-t628) were used to probe the importance of this region on the regulation of hormonal responsiveness. The chosen cells line express comparable densities of cell surface rLHR, bind human CG (hCG) with high affinity, and respond to hCG with increases in cAMP and inositol phosphate accumulation. Cells expressing rLHR-wt or rLHR-t653 responded to hCG, or phorbol 12-myristate-13-acetate (PMA) stimulation with a similar increase in rLHR phosphorylation. Neither of these two stimuli increased rLHR phosphorylation in cells expressing rLHR-t631 or rLHR-t628, however. The cell line expressing rLHR-t653, the phosphorylation-positive receptor mutant, desensitized normally in response to PMA or hCG stimulation. This truncated form of rLHR also was down-regulated normally in response to hCG stimulation. In contras...