A honey bee becomes a royal queen or a common worker as a result of the food she receives as a larva. While it has been well established that royal jelly is the diet that makes bees queens, the molecular path from food to queen is still in dispute.

However, scientists at Arizona State University, led by Adam Dolezal and Gro Amdam, have helped reconcile some of the conflicts about bee development and the role of insulin pathways and partner proteins. Their article "IIS and TOR nutrient-signaling pathways act via juvenile hormone to influence honey bee cast fate" has been published in the December issue of the Journal of Experimental Biology.

Central to the dispute within the scientific community about “who would be queen” has been a groundbreaking study published in the journal Nature by Japanese scientist Masaki Kamakura in 2011. He found that a single protein in royal jelly, called royalactin, activated queen development in larval bees through interaction with an epidermal growth factor receptor (EGFR). Kamakura’s work suggested that insulin signals do not play a role in queen development, despite previous studies suggesting otherwise, including work pioneered with the insulin receptor protein by Amdam’s group.

Undeterred by Kamakura’s findings, Dolezal, a doctoral student, and Amdam, a Pew Biomedical Scholar and professor in ASU’s School of Life Sciences, looked for ways to resolve the disparity between the research studies. Funded by the National Science Foundation, Amdam’s team’s first step involved taking control of the insulin receptor’s partner protein, IRS, which the insulin receptor relies upon for signaling.

The scientists found that by blocking IRS, they caused a central developmental hormone to crash, which forced larval bees into the worker mold despite their diet of royal jelly. Amdam’s team then “rescued” the now worker-destined bees. They found that by giving the bees hormone treatments, the bees could then develop along the queen trajectory.