Bees are cool. Supersocieties, domestication, the waggle dance and delicious sweet honey. And now this: Royalactin induces queen differentiation in honeybees.
For a long time, the existence of 'castes' (worker, queen, soldier etc.) in social insects has been a subject of much thought by biologists. Clearly all members of a hive have the same genome, so the fact that individuals have such varied appearance (and that this is very predictable - all workers are more or less identical, but very different from queens etc.) is a compelling argument for the primacy of environmental factors in development. The difference between workers and queens is obviously not genetic (in the bases of the DNA itself) but turns out to be epigenetic. The DNA in the nucleus of a cell is wrapped around proteins called histones. These histones can be modified by other enzymes which affects the interactions between neighbouring histones and alters the level of activity of nearby genes by altering the accessibility of particular DNA residues.
All female bee larvae are 'born' equal (there is no difference between worker and queen embryos - they are equivalent). What determines the developmental trajectory of a young bee larva is the amount of royal jelly it is fed. Something in the royal jelly produced by worker bees causes the histones to be altered differently in worker and queen embryos, leading to differences in gene expression, leading to changes in development leading to very different adult forms.
The paper this week from Masaki Kamakura goes looking for what exactly it is in the royal jelly that has this queen-making potential. By very carefully analysing royal jelly, by testing its components individually for the ability to evoke 'royal' changes (such as increased growth and larger ovaries), it is possible to demonstrate that the action of royal jelly is due to a previously described protein named royalactin. Obviously, this is an interesting finding, but to corroborate royalactin as the crucial factor, we would like to know something about the mechanism by which its ingestion can bring about the profound developmental changes necessary to produce a queen bee rather than a worker.
Kamakura does this by making queen flies.
The fruit fly Drosophila melanogaster is a model organism for many biological processes and is here used as a perfect model of bee development. When Drosophila larvae were fed on a diet of 20% royal jelly in addition to their normal food, the adult flies showed many similarities with queen bees (quicker development, larger size, higher egg production and a longer life). The picture at the top of this post is from the paper. The fly on the left is a normal female, whereas the fly on the right was fed on the 20% royal jelly diet, clearly showing the increased size.
Kamakura examines the effects of feeding some mutant strains of Drosophila the royal jelly diet. Flies with defects in the Egfr signalling pathway do not show the 'queen fly' effect, suggesting that royalactin acts via this pathway. He also engineered flies to express royalactin themselves and demonstrates once again that this protein can cause the queen fly effect and that the Egfr pathway seems to be involved. Finally, Kamakura knocks out the EGFR pathway in developing bees using a technique called RNA-interference and shows that when EGFR signalling is inactivated, individuals fed royal jelly do not develop perfectly as queens.
This is a very interesting piece of work, thoroughly deserving of a place in Nature. We can see the conservation of signalling systems between bees and flies and can imagine how caste differentiation in bees could have evolved - existing developmental pathways are subtly modified to give a new phenotype. The ability of one genome to produce multiple alternative forms in different contexts is conclusive proof of the importance of developmental plasticity both in the short-term (development of indivduals) and on a much larger evolutionary scale (in the appearance of new features and traits).
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