No abstract

Multiple harmful factors cause chronic sub-lethal stress in managed honey bee colonies. In weak colonies, worker bees may not efficiently maintain the optimum temperature (33-36°C) in peripheral brood development areas. A short period at 25°C induces physiological adjustments and increases the mortality in honey bee brood reared in vitro . Molecular damage due to oxidative imbalance can be one of the main causes of mortality when organisms are under stress. Here, we demonstrate that in vitro rearing honey bee brood exposed 3 days at suboptimal temperature (25°C) does not lead to H 2 O 2 accumulation and oxidative protein damage. Cold-stressed honey bee brood showed increased levels of both total antioxidant status (TAS) and expression of peroxiredoxins PRX1 and PRX4 , but not of catalase activity. Results indicate that specific antioxidant defenses induced in honey bee brood under moderated cold stress are enough to keep H 2 O 2 levels under control and avoid major protein damages. It is concluded that the increase of mortality in cold-stressed brood are due to multifactor's, beyond uncontrolled oxidative injuries. honey bee brood / cold stress / oxidative damage / antioxidant responses

30In temperate climates, low ambient temperatures in late winter and in spring can result in cold 31 stress conditions in brood areas of weakened honey bee colonies, leading to increased levels 32 of developmental interruptions and death of the brood. Very little is known about the 33 physiological and molecular mechanisms that regulate honey bee brood responses to acute 34 cold-stress. Here, we hypothesized that central regulatory pathways mediated by 35 insulin/insulin-like peptide signalling (IIS) and adipokinetic hormone (AKH) are linked to 36 metabolic changes in cold-stressed honey bee brood. A. mellifera brood reared at suboptimal 37 temperatures showed diminished growth rate and arrested development progress. Notably, 38 cold-stressed brood rapidly recovers the growth in the first 24 h after returning at control 39 rearing temperature, sustained by the induction of compensatory mechanisms. We 40 determined fast changes in the expression of components of IIS and AKH pathways in cold-41 stressed brood supporting their participation in metabolic events, growth and stress 42responses. We also showed that metabolic rate keeps high in brood exposed to stress 43 suggesting a role in energy supply for growth and cell repair. Additionally, transcript levels of 44 the uncoupling protein MUP2 were elevated in cold-stressed brood, suggesting a role for heat 45 generation through mitochondrial decoupling mechanisms and/or ROS attenuation. 46Physiological, metabolic and molecular mechanisms that shape the responses to cold-stress 47 in honey bee brood are addressed and discussed. 48 49 50 51 52 53 54 55 56 3 57