Honey bees (Apis mellifera) are key pollinators, playing a vital role in ecosystem maintenance and stability of crop yields. Recently, reduced honey bee survival has attracted intensive attention. Among all other honey bee stresses, temperature is a fundamental ecological factor that has been shown to affect honey bee survival. Yet, the impact of low temperature stress during capped brood on brood mortality has not been systematically investigated. In addition, little was known about how low temperature exposure during capped brood affects subsequent adult longevity. In this study, capped worker broods at 12 different developmental stages were exposed to 20°C for 12, 24, 36, 48, 60, 72, 84 and 96 hours, followed by incubation at 35°C until emergence. We found that longer durations of low temperature during capped brood led to higher mortality, higher incidences of misorientation inside cells and shorter worker longevity. Capped brood as prepupae and near emergence were more sensitive to low-temperature exposure, while capped larvae and mid-pupal stages showed the highest resistance to low-temperature stress. Our results suggest that prepupae and pupae prior to eclosion are the most sensitive stages to low temperature stress, as they are to other stresses, presumably due to many physiological changes related to metamorphosis happening during these two stages. Understanding how low-temperature stress affects honey bee physiology and longevity can improve honey bee management strategies.

Young larvae of the honey bee (Apis mellifera) are totipotent; they can become either queens (reproductives) or workers (largely sterile helpers). DNA methylation has been shown to play an important role in this differentiation. In this study, we examine the contributions of diet and cell size to caste differentiation. We measured the activity and gene expression of one key enzyme involved in methylation, Dnmt3; the rates of methylation in the gene dynactin p62; as well as morphological characteristics of adult bees developed either from larvae fed with worker jelly or royal jelly; and larvae raised in either queen or worker cells. We show that both diet type and cell size contributed to the queen-worker differentiation, and that the two factors affected different methylation sites inside the same gene dynactin p62. We confirm previous findings that Dnmt3 plays a critical role in honey bee caste differentiation. Further, we show for the first time that cell size also plays a role in influencing larval development when diet is kept the same.

Varroa (Varroa destructor) has recently become resistant to Apistan, a pyrethroid pesticide with tau-fluvalinate as its active ingredient. In many insect pests, resistance to pyrethroid insecticides is due to reduced target-site (sodium channel) sensitivity to pyrethroids in the nervous system, a phenomenon called knockdown resistance (kdr). A number of studies showed that kdr and kdr-type resistance is a result of point mutations in the para family of sodium channel genes. To investigate the molecular mechanism of resistance to fluvalinate in varroa, we have cloned and sequenced a large cDNA fragment corresponding to segment 3 of domain II (IIS3) to segment 6 of domain IV (IVS6) of a para-homologous sodium channel gene (VmNa) from susceptible and resistant mite populations. The deduced amino acid sequence from this cDNA shares 71%, 60%, and 50% identity with the corresponding region of the para-homologous protein of the Southern cattle tick, Boophilus microplus, Drosophila melanogaster Para, and rat brain type II sodium channel α-subunit, respectively. Sequence analysis revealed that four amino acid changes, F758L in IIIS6, L826P in the linker connecting domains III and IV, I982V in IVS5 and M1055I in IVS6, were correlated with fluvalinate resistance in both Florida and Michigan populations. Interestingly, the kdr or super-kdr (which confers much higher level resistance than kdr) mutation previously identified in insects was not detected in the resistant mites. These results support the emerging notion that distinct sodium channel gene mutations are selected in different insects and arachnids in response to pyrethroid selection.

The Varroa mite, Varroa destructor, is an acarine ecto-parasite on Apis mellifera. It is the worst pest of Apis mellifera, yet its reproductive biology on the host is not well understood. In particular, the significance of the phoretic stage, when mites feed on adult bees for a few days, is not clear. In addition, it is not clear whether the preference of mites for nurses observed in the laboratory also happens inside real colonies. We show that Varroa mites prefer nurses over both newly emerged bees and forgers in a colony setting. We then determined the mechanism behind this preference. We show that this preference maximizes Varroa fitness, although due to the fact that each mite must find a second host (a pupa) to reproduce, the fitness benefit to the mites is not immediate but delayed. Our results suggest that the Varroa mite is a highly adapted parasite for honey bees.