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Key Event Title
Abnormal, Role change within caste
|Level of Biological Organization|
Key Event Components
Key Event Overview
AOPs Including This Key Event
|AOP Name||Role of event in AOP||Point of Contact||Author Status||OECD Status|
|nAChR activation - colony loss 7||KeyEvent||Carlie LaLone (send email)||Open for comment. Do not cite|
|nAChR activation - colony loss 5||KeyEvent||Carlie LaLone (send email)||Open for comment. Do not cite|
|Nosema to role change to colony loss/failure||KeyEvent||Carlie LaLone (send email)||Under Development: Contributions and Comments Welcome|
Key Event Description
Text from LaLone et al. (2017) Weight of evidence evaluation of a network of adverse outcome pathways linking activaiton of the nicotinic acetylcholine receptor in honey bees to colony death. Science of the Total Environment 584-585, 751-775:
"Like most eusocial insects, honey bees exhibit age-based division of labor and progress from nurse to forager as they age (Seeley, 1982). This type of age-related behavioral change termed age polyethism, is a genomically, nutritionally, and hormonally controlled process (Ament et al., 2010; Cheng et al., 2015). Such behavior changes in adult worker bees occur in a predictable sequence as theymove fromcentrally located in-hive activities including cleaning brood cells (0–5 d old), to feeding brood, capping brood, trimming cappings, and attending the queen (2–11 d old), to peripherally located in-hive activities, such as grooming nest-mates, feeding nest-mates, ventilating the hive, producing wax and shaping comb cells, receiving and storing nectar, packing pollen, and processing nectar into honey and pollen into bee bread (11–20 d old), to outside activities, including guarding the hive and foraging (20+ d old) (Seeley, 1982). However, honey bees exhibit phenotypic plasticity whereby the rate of behavioral change is highly flexible, meaning that under different scenarios, based on colony needs, bees will accelerate or reverse their behavioral development. For example, to compensate for a loss of foragers, disease, or nutritional stress, bees will initiate precocious (early behavioral development) foraging (Cheng et al., 2015; Huang and Robinson, 1996). It is biologically plausible that early initiation of foraging could lead to a shortage of hive bees needed to tend to the brood, which could hinder development of the brood. In addition, precocious foraging is correlated with shorter lifespans. Therefore, bees that forage earlier tend to do so at the expense of their longevity which could impact overall colony resource acquisition and productivity (Woyciechowski and Moroń, 2009). However, the relationship may be complex given that with seasonal variation, food availability, predation pressures, and adverse weather conditions that promote greater in-hive activity, older foragers can reverse their behavior, regenerate hypopharyngeal glands, and assume roles within the hive (Huang and Robinson, 1996). Behavioral plasticity is driven, in part, by juvenile hormone (JH) and its interplay with Vtg, acting together in a feed-back loop to control the onset of labor tasks, such as foraging (Page et al., 2012). For example, high Vtg levels suppress JH, delaying onset of foraging behavior,whereas high JH suppresses Vtg, causing a decrease in nursing behavior (Page et al., 2012). Studies exploring drivers of precocious foraging, using both treatment with a JH analog and social manipulation of a single-cohort colony of 1 d old bees in the absence of older foragers, induced precocious foraging, demonstrating that both hormonal and social interactions play a role (Chang et al., 2015; Perry et al., 2015). Active foragers produce a pheromone, ethyl oleate, which is transferred to the hive bees during trophallaxis or oral food exchange, delaying the rate at which bees transition to foraging. Therefore, if the number of foragers diminishes, recruitment to foraging can be accelerated. Additionally, allatectomy (removal of the corpora allata glands that produce JH) led to the discovery that JH is involved in modulating the speed at which bees develop into foragers, but not in activation of foraging itself (Sullivan et al., 2003). However, studies using ribonucleic acid
interference (RNAi) to knockdown Vtg production have found the protein to have a prominent role in the initiation of honey bee foraging, causing an increase in JH titer and extreme precocious foraging (3 d old bees) (Guidugli et al., 2005; Marco Antonio et al., 2008). Vitellogenin is synthesized in fat body cells, released to the hemolymph (circulation), and taken up in developing oocytes (Corona et al., 2007). Mature honey bee queens, which lay ~1000 eggs/day, continuously synthesize Vtg at high levels, including during periods when egg laying ceases (Seehuus et al., 2006; Corona et al., 2007). However, in sterile worker bees, Vtg levels have been shown to change throughout their lives, with the highest levels observed in the long-lived winter bees and lowest in the short-lived summer foragers (Münch et al., 2015). In addition to the role Vtg plays as an egg yolk protein, it has a role in oxidative stress resistance (Corona et al., 2007; Seehuus et al., 2006; Amdam et al., 2004)."
How It Is Measured or Detected
Text from Table 2 in LaLone et al. (2017) Weight of evidence evaluation of a network of adverse outcome pathways linking activaiton of the nicotinic acetylcholine receptor in honey bees to colony death. Science of the Total Environment 584-585, 751-775:
"• Age of first forage • Hypopharyngeal gland development in forage bees that revert to hive bees"
Domain of Applicability
LaLone, C.A., Villeneuve, D.L., Wu-Smart, J., Milsk, R.Y., Sappington, K., Garber, K.V., Housenger, J. and Ankley, G.T., 2017. Weight of evidence evaluation of a network of adverse outcome pathways linking activation of the nicotinic acetylcholine receptor in honey bees to colony death. STOTEN. 584-585, 751-775.
Seeley, T.D., 1982. Adaptive significance of the age polyethism schedule in honeybee colonies. Behav. Ecol. Sociobiol. 11 (4), 287–293.
Ament, S.A., Wang, Y., Robinson, G.E., 2010. Nutritional regulation of division of labor in honey bees: toward a systems biology perspective. Wiley Interdiscip. Rev. Syst. Biol. Med. 2 (5), 566–576.
Cheng, L.H., Barron, A.B., Cheng, K., 2015. Effects of the juvenile hormone analogue methoprene on rate of behavioural development, foraging performance and navigation in honey bees (Apis mellifera). J. Exp. Biol. 218, 1715–1724.
Huang, Z.Y., Robinson, G.E., 1996. Regulation of honey bee division of labor by colony age demography. Behav. Ecol. Sociobiol. 39 (3), 147–158.
Woyciechowski, M., Moroń, D., 2009. Life expectancy and onset of foraging in the honeybee (Apis mellifera). Insect. Soc. 56 (2), 193–201.
Page Jr., R.E., Rueppell, O., Amdam, G.V., 2012. Genetics of reproduction and regulation of honeybee (Apis mellifera L.) social behavior. Annu. Rev. Genet. 46, 97–119.
Chang, L.H., Barron, A.B., Cheng, K., 2015. Effects of the juvenile hormone analogue methoprene on rate of behavioural development, foraging performance and navigation in honey bees (Apis mellifera). J. Exp. Biol. 218 (11), 1715–1724.
Perry, C., Søvik, E., Myerscough, M.R., Barron, A.B., 2015. Rapid behavioral maturation accelerates failure of stressed honey bee colonies. Proc. Natl. Acad. Sci. U. S. A. 112 (11), 3427–3432.
Sullivan, J.P., Fahrbach, S.E., Harrison, J.F., Capaldi, E.A., Fewell, J.H., Robinson, G.E., 2003. Juvenile hormone and division of labor in honey bee colonies: effects of allatectomy on flight behavior and metabolism. J. Exp. Biol. 206 (13), 2287–2296.
Guidugli, K.R., Nascimento, A.M., Amdam, G.V., Barchuk, A.R., Omholt, S., Simões, Z.L.P., Hartfelder, K., 2005. Vitellogenin regulates hormonal dynamics in the worker caste of a eusocial insect. FEBS Lett. 579, 4961–4965.
Marco Antonio, D.S., Guidugli-Lazzarini, K.R., do Nascimento, A.M., Simões, Z.L., Harfelder, K., 2008. RNAi-mediated silencing of vitellogenin gene function turns honeybee (Apis mellifera) workers into extremely precocious foragers. Naturwissenschaften 95 (10), 953–961.
Corona,M., Velarde, R.A., Remolina, S.,Moran-Lauter, A.,Wang, Y., Hughes, K.A., Robinson, G.E., 2007. Vitellogenin, juvenile hormone, insulin signaling, and queen honey bee longevity. Proc. Natl. Acad. Sci. 104 (17), 7128–7133.
Seehuus, S.C., Norberg, K., Gimsa, U., Krekling, T., Amdam, G.V., 2006. Reproductive protein protects functionally sterile honey bee workers from oxidative stress. PNAS 103 (4), 962–967.
Amdam, G.V., Simões, Z.L., Hagen, A., Norber, K., Schrøder, K., Mikkelsen, Ø., Kirkwood, T.B., Omholtk, S.W., 2004. Hormonal control of the yolk precursor vitellogenin regulates immune function and longevity in honeybees. Exp. Gerontol. 39 (5), 767–773.