Aedes aegypti pharate 1st instar quiescence affects larval fitness and metal tolerance

The eggs of the mosquito Aedes aegypti possess the ability to undergo an extended quiescence hosting a fully developed 1st instar larvae within the chorion. As a result of this life history trait pharate larvae can withstand months of quiescence inside the egg where they depend on stored maternal reserves. A. aegypti mosquitoes are frequently associated with urban habitats that may contain significant metal pollution. Therefore, the duration of quiescence and extent of nutritional depletion may affect the physiology and survival of larvae that hatch in a suboptimal habitat. The aim of this study was to determine the effect of an extended quiescence on larval nutrient reserves and the subsequent effects of metal exposure on larval fitness, survival and development. We hypothesized that an extended quiescence would reduce nutritional reserves and alter the molecular response to metal exposure thereby reducing larval survival and altering larval development. As a molecular marker for metal stress responses, we evaluated transcriptional changes in the metallothionein gene (AaMtn) in response to quiescence and metal exposure. Extended 1st instar quiescence resulted in a significant decrease in lipid reserves and negatively affected larval fitness and development. AaMtn transcription and metal tolerance were compromised in first instars emerged from eggs that had undergone an extended quiescence. These findings suggest that newly emerged mosquito larvae that had survived a relatively long pharate 1st instar quiescence (as might occur during a dry season) are more vulnerable to environmental stress. Pharate 1st instar quiescence could have implications for vector control strategies. Newly emerged mosquito larvae at the end of the dry season or start of the wet season are physiologically compromised, and therefore potentially more susceptible to vector control strategies than mosquito larvae hatched subsequently throughout the wet season. Published by Elsevier Ltd.