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. Author manuscript; available in PMC: 2011 May 1.
Published in final edited form as: Anim Behav. 2010 May;79(5):973–980. doi: 10.1016/j.anbehav.2010.02.007

Figure 4.

Figure 4

The reproductive ground plan hypothesis (RGPH) underscores that vitellogenin (black bars) and juvenile hormone (JH, grey arrow-bars) modules are inherent to insect reproduction (Amdam et al. 2007). Reproductive biology is influenced by environmental factors such as food availability sensed by nutrient-sensitive pathways (green). These pathways include the insulin receptor substrate (IRS) and target of rapamycin (TOR); while PDK1 is a phosphorylation target downstream of both IRS and TOR. The response is integrated by endocrine signal transmission via systemic hormones like JH and nuclear hormone receptors such as USP (blue) and HR46 (46, purple). The double repressor hypothesis (DRH) (Amdam & Omholt 2003) proposes that transition from nursing (mid panels) to foraging behaviour (right panels) in honeybees is influenced by a feedback loop (red (−) arrows) between vitellogenin and JH. Vitellogenin inhibits JH synthesis, USP expression and insulin-like signalling (Guidugli et al. 2005; Hunt et al. 2007; Ament et al. 2008) that are increased in foragers. When vitellogenin levels drop, JH can be triggered to increase and further suppress expression of its own repressor. We propose that bidirectional selection on pollen-hoarding behaviour acted on these relationships. (a) In high pollen-hoarding strain bees, nutrient sensing and reproductive endocrine signal transmission is increased, resulting in developmental retention of a larger ovary (filament structures inside larva, top left panel) and dynamic interplay between the ovary, vitellogenin, and adult behaviour (top mid (nurse) versus top right (forager) panel). (b) In low strain bees, nutrient sensing and reproductive endocrine signal transmission is less active (shown as less intense green and red indicators), resulting in reduced ovary size (fewer filaments retained inside larva, bottom left panel) and less sensitivity of interplay between ovary, vitellogenin, and behaviour in adults (bottom mid versus bottom right panel). Increased HR46 expression (Wang et al. 2009) might be central to the low strain phenotype, as this receptor has potential to competitively inhibit the signal transmission of JH and USP.