Microarrays reveal discrete phases in juvenile hormone regulation of mosquito reproduction

Abstract

Mosquitoes are vectors of some of the world’s most devastating human diseases: malaria, dengue fever, and yellow fever in the tropics, and encephalitis and West Nile virus in the United States. The female mosquito usually requires a blood meal before she makes a batch of eggs, and one for each subsequent batch thereafter. This repeated blood feeding makes her an exceptional disease vector, picking up a pathogen with one blood meal and then transmitting it on successive meals. After emergence (eclosion) as an adult, the female must mature before she can produce eggs in response to the blood meal. This maturation is initiated by an insect-specific juvenile hormone (JH), a sesquiterpenoid that acts on the fat body (the liver and the adipose tissue of the insect) to increase both its metabolic machinery and its protein-synthesizing capacity so that it can synthesize the yolk protein vitellogenin in response to the blood meal (Fig. 1) (1). JH also directs previtellogenic development of the ovary. In PNAS, Zou et al. (2) show, using microarray analysis, that JH controls the maturation of the fat body of the yellow fever, dengue mosquito Aedes aegypti in a time-dependent manner by regulating three major gene clusters. Early-posteclosion (EPE) gene expression peaks at 6 h, mid-posteclosion (MPE) genes at 24 h, and late-posteclosion (LPE) genes at 66 h after eclosion (Fig. 1). These times correspond to low, intermediate, and high JH titers because JH secretion begins at eclosion and peaks at 36 h (3). The EPE and MPE genes are primarily involved in carbohydrate and lipid metabolism, whereas the late genes are primarily for the buildup of the protein-synthesizing machinery based on gene ontology, as discussed below.