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The parathyroid hormone-related peptide (PTHrP) gene has been reported to be subject to a wide variety of physiological and pharmacological controls. Two distinct patterns of PTHrP mRNA response have been recognized, one characterized by a prolonged or plateau response lasting many hours to days and the second characterized by rapid induction-deinduction kinetics and lasting 1 to several hours. The kinetics of the second pattern are similar to those displayed by primary response genes like nuclear protooncogenes, cytokines, and growth factors. In GH4C1 rat pituitary cells, 17 beta-estradiol induced a rapid and transient increase in PTHrP mRNA expression, with a peak response at 1-2 h. This response appeared to be due to a rapid and transient burst in gene transcription, which by runoff analysis was maximal at 20-40 min and declined thereafter. PTHrP mRNA half-life was 30 min in these cells and was unaltered by estradiol. Cycloheximide did not block the 17 beta-estradiol-induced response but rather prolonged it, and runoff analysis revealed that this effect was due to a prolongation or persistence of PTHrP gene transcription. These findings suggest that the transient nature of the native response reflects the effects of an estrogen-inducible repressor. All of these features are characteristic of a prototypical primary response gene.

The sections in this article are: 1 Intracellular Transport in Vesicles 2 Membrane Fusion and Exocytosis 2.1 Investigations in Synaptic Vesicles 2.2 Investigations in Yeast 2.3 Reconstituted Systems of Transport 2.4 Convergence of Separate Approaches 2.5 Calcium Dependence of Stimulated Neurotransmitter Release 2.6 Docking Vesicles to the Correct Membrane 2.7 Other Fusion Mechanisms 2.8 Evidence for SNAP-NSF-Mediated Docking/Fusion With Dense Core Granules 2.9 Exocytosis in Endocrine Cells 3 Membrane Budding and Endocytosis 3.1 Budding Involving Clathrin 3.2 Budding Involving COPI/ARF 3.3 Endocytosis in Endocrine Cells 3.4 Formation of Secretory Granules in Endocrine Cells