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Enter Arizona Lab

Amdam lab, Department of Chemistry, Biotechnology and Food Science, Norwegian University of Life Sciences

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Our goal is to understand the plasticity of honey bee aging, with focus on aging regulation and senescence of the brain. In collaboration with the groups of Drs. Zilá L.P. Simões and Klaus Hartfelder, University of São Paulo, Ribeirão Preto, Brazil, we have identified a regulatory pathway that can determine honey bee longevity. This pathway incorporates a systemic hormone, juvenile hormone, and the gene vitellogenin, which encodes a major reproductive (yolk) protein precursor that is conserved between oviparous species. In D. melanogaster, juvenile hormone shortens life as part of the insulin/insulin-like growth factor signaling (IIS) pathway that co-regulates somatic maintenance and reproduction antagonistically. In C. elegans, the vitellogenin protein encoding genes vit-2 and vit-5 are downstream of the IIS receptor Daf-2, and also have negative effects on lifespan. Yet, the regulatory action of juvenile hormone on vitellogenin activity is inverted in honey bees, and we have found that this vitellogenin has functions not identified in other species. First, the worker caste is characterized by a positive feedback loop in which vitellogenin affects the hormonal control system to suppress the systemic juvenile hormone level. Second, this vitellogenin can prolong life also as a scavenger of free radicals, thereby protecting the bee against oxidative stress damage (an established marker of aging). As vitellogenin levels primarily are functions of the bees’ social roles, this relationship suggests that honey bee aging is best explained by social function rather than by chronological age.