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United States Department of Agriculture

Agricultural Research Service

Title: Ecdysteroid Regulation of Salivary Gland Degeneration in the Ixodid Tick, Amblyomma Hebraeum: a Potential Role for Oxoecdysteroid 3 Beta-Reductase

item Lomas, Lee - UNIV OF LIVERPOOL
item Gelman, Dale
item Kaufman, W - UNIV OF ALBERTA

Submitted to: General and Comparative Endocrinology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: October 13, 1997
Publication Date: N/A

Interpretive Summary: Ticks, well-known vectors of disease-causing organisms, transmit pathogens to their host during the process of feeding. The endocrinology of salivary gland function and degeneration, integral parts of tick feeding, is not well-understood. Lack of knowledge in this area impedes the development of biorational tick control agents. Results of this research clarify the role of ecdysteroids and enzymes which metabolize these ecdysteroids in salivary gland degeneration. This information should be useful to other scientists investigating the endocrinology of tick salivary gland function and its relationship to ovarian development.

Technical Abstract: Salivary gland degeneration in the female tick, Amblyomma hebraeum Koch, is triggered by an ecdysteroid (ES) hormone. Under both in vivo and in vitro conditions, it requires 4 days for completion. In partially fed females that have fed beyond a 'critical weight', the commitment period for salivary gland degeneration occurs between 24 and 48 h after removal from the host. Although tissue degeneration begins with 24 h post- engorgement, ES titre as measured by radioimmunoassay (RIA) does not rise to threshold levels until 48 h post engorgement. To explain this anomaly, we examined two hypotheses: (1) there is an early hormonal signal (3-dehydroecdysone; 3DE) which is an ES not detectable by the antibody used in our RIA and (2) the low hemolymph titre during the first two days post-engorgement is not an accurate reflection of the ES concentration within the tissue itself. 3-Oxoecdysteroid 3 beta-reductase (ketoreductase) was present in salivary glands, but neither ketoreductase nor 3DE was detected in hemolymph. The ES content of salivary gland homogenates was similar to that of the hemolymph while that of saliva was undetectable. Together, these results support our second hypothesis that the metabolically active tissue of the salivary gland is exposed to a much higher concentration of ES than is present in the hemolymph.

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