Abstract
The titer of juvenile hormone (JH), which has wide ranging physiological effects in insects, is regulated in part by JH esterase (JHE). We show that overexpression in Drosophila melanogaster of the JHE binding protein, DmP29 results in a series of apparent anti-JH effects. We hypothesize that DmP29 functions in transport of JHE such that over- or under-expression of DmP29 results in increased or decreased JH degradation at specific sites respectively. Overexpression of DmP29 during the first or second instar was lethal, while overexpression during the third instar resulted in eclosion of small adults. Overexpression of DmP29 in newly eclosed flies reduced ovarian development and fecundity in addition to reducing the abundance of aggregation pheromone (cis-vaccenyl acetate) in males and courtship pheromone (cis,cis-7,11-heptacosadiene) in females. Both sexes also had lower levels of 23 and 25 carbon monoenes. Females exhibited reduced receptivity to mating, and males exhibited male-male courtship behavior, with both sexes being hyperactive: Male flies covered 2.7 times the distance of control flies at 2.9 times the maximum velocity. Application of the JH analog methoprene reversed impaired ovarian development, supporting a role for reduced JH in production of this phenotype. Rather than increasing lifespan as expected from a JH deficiency, overexpression of DmP29 reduced the life span of adult flies which may result from the hyperactivity of these flies. Underexpression of DmP29 resulted in reduced longevity, increased fecundity and reduced titers of pupal JHE. An alternative hypothesis, that mitochondrial dysfunction rather than JHE results in the JH-mediated phenotypes, is discussed.
