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ARS Home » Pacific West Area » Tucson, Arizona » Honey Bee Research » Research » Publications at this Location » Publication #319741

Research Project: Determining the Impacts of Pesticide- and Nutrition-Induced Stress on Honey Bee Colony Growth and Survival

Location: Honey Bee Research

Title: Transcriptional, translational, and physiological signatures of undernourished honey bees (Apis mellifera) suggest a role for hormonal factors in hypopharyngeal gland degradation

Author
item Corby-harris, Vanessa
item Meador, Charlotte
item Snyder, Lucy
item Schwann, Melissa - Former ARS Employee
item Maes, Patrick - University Of Arizona
item Jones, Beryl - University Of Illinois
item Walton, Alexander - Iowa State University
item Anderson, Kirk

Submitted to: Journal of Insect Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/30/2015
Publication Date: 1/2/2016
Citation: Corby-Harris, V.L., Meador, C.A., Snyder, L.A., Schwann, M., Maes, P., Jones, B., Walton, A., Anderson, K.E. 2016. Transcriptional, translational, and physiological signatures of undernourished honey bees (Apis mellifera) suggest a role for hormonal factors in hypopharyngeal gland degradation. Journal of Insect Physiology. 85:65-75. doi: 10.1016/j.jinsphys.2015.11.016.

Interpretive Summary: Nurse worker bees take care of young bees and the queen in the hive by secreting royal and worker jelly from glands in their head. The size that these glands grow to is dependent on many factors, including diet; bees fed low amounts of protein and/or pollen have smaller glands that well-nourished bees. Glands start growing by 3d of adult age and up to this age are of similar size irrespective of their diet. However, in a very small window of early adulthood, differences in gland size start to emerge. This led us to the question of whether glands simply don’t grow or if they do grow and are actively degraded in this window. Through a combination of gene and protein studies and physiological assays we find support for the latter hypothesis. In addition, we find evidence that many of the same pathways that control gland growth in other insects also operate in bees. This work is relevant because it demonstrates why gland size responds to diet but also allows us to target specific pathways to increase gland size or at least prevent their degradation in colonies so nurse bees can properly nourish hive larvae under stressful conditions.

Technical Abstract: Honey bee colonies function as a superorganism, where facultatively sterile female workers perform various tasks that support the hive. Nurse workers undergo numerous anatomical and physiological changes in preparation for brood rearing, including the growth of hypopharyngeal glands (HGs). These glands secrete a protein- and lipid-rich jelly used to sustain developing larvae. Pollen availability is positively correlated with gland growth, but growth in the first three days is similar regardless of diet, suggesting that initial growth is a pre-determined process while later development depends on nutrient availability during a critical window in early adulthood (3-8d). It is unclear whether the resultant size differences in nurse HG are simply due to growth stasis or active degradation of the tissue via apoptosis and autophagy. To determine the processes regulating HG size, we measured all differentially expressed gene transcripts and proteins in the HGs from 8d old bees that were well-nourished (fed pollen) or undernourished (fed no pollen). Undernourished bees had the highest rate of differential genes expression, with affected processes including salivary gland apoptosis, oogenesis, and ecdysteroid-mediated hormone signaling were among those up-regulated in the HGs of undernourished bees. Protein secretion was virtually the only process up-regulated in well-nourished bees. Undernourished bees also had higher ecdysteroid levels and phosphatase activity, a physiological marker of cell death, compared to well-nourished bees. These results suggest that HG degradation is an active process regulated by the same ecdysteroid signaling that regulates salivary gland development and oogenesis in non-social taxa.