Role of calcium in the stimulation of ecdysteroidogenesis by recombinant prothoracicotropic hormone in the prothoracic glands of the silkworm, Bombyx mori

• Published in: Insect biochemistry and molecular biology 1998-11, Vol.28 (11), p.861-867
• Main Authors: Gu, Shi-Hong, Chow, Yien-Shing, O'Reilly, David R
• Format: Article
• Language: English
• Subjects: Bombyx mori; cAMP Ca 2+ channel; Ecdysteroid secretion; Recombinant PTTH; Silkworms
• ISSN: 0965-1748; 1879-0240
• DOI: 10.1016/S0965-1748(98)00074-5

The aim of this study was to clarify whether Ca 2+ plays a role in the mechanism by which recombinant prothoracicotropic hormone (PTTH) stimulates ecdysteroidogenesis by the prothoracic glands of the silkworm, Bombyx mori. Omission of Ca 2+ from the incubation medium, or inclusion of a Ca 2+ channel blocker (verapamil or lanthanum) did not affect basal ecdysteroid secretion, but greatly inhibited the stimulation of ecdysteroidogenesis by PTTH. The addition of a Ca 2+ ionophore (ionomycin or A23187) stimulated ecdysteroid secretion in a dose-dependent manner. Furthermore, thapsigargin, a potent Ca 2+-ATPase inhibitor, enhanced ecdysteroid secretion. In contrast, thimerosal, a thiol-oxidizing reagent, inhibited prothoracic gland activity. The mechanism of Ca 2+ action was examined further in relation to the cAMP effector system. Ca 2+ deprivation greatly suppressed the accumulation of cAMP in prothoracic glands treated with PTTH but had no effect on basal levels. Omission of Ca 2+ from the incubation medium, or inclusion of a Ca 2+ channel blocker (verapamil or lanthanum) did not affect the stimulation of ecdysteroid secretion in response to dibutyryl cAMP or 1-methyl-3-isobutylxanthine. The present study suggests that specific regulatory actions of Ca 2+ in prothoracic gland cells are exerted prior to cAMP generation.