In honey bee colonies the queen is the only fertile female. She lays all the eggs. The worker bees are female but sterile. The process of ovulation in worker bees is suppressed in response to phermomes. This is an example of genetic altruism where the reproductive benefit of worker bees is suppressed in favor of the good of the hive. There are good theories about why this would ultimately benefit the workers.
In some hives, a few worker bees can lay eggs and these eggs will hatch. The presence of "cheaters" in an altruistic society is expected and normal. Oxley et al. (2008) looked at the DNA from these "cheater" hives and compared it to the DNA from bees that were sterile. The idea was to identify the gene responsible for suppressing ovulation in workers; presumably that gene was somehow different in the hives with "cheaters."
Here's the abstract of the paper.
The all-female worker caste of the honey bee (Apis mellifera) is effectively barren in that workers refrain from laying eggs in the presence of a fecund queen. The mechanism by which workers switch off their ovaries in queenright colonies is pheromonally cued, but there is genetically-based variation among individuals: some workers have high thresholds for ovary activation, while for others the response threshold is lower. Genetic variation for threshold response by workers to ovary-suppressing cues is most evident in "anarchist" colonies in which mutant patrilines have a proportion of workers that activate their ovaries and lay eggs, despite the presence of a queen. In this study we use a selected anarchist line to create a backcross queenright colony that segregated for high and low levels of ovary activation. We used 191 informative microsatellite loci, covering all 16 linkage groups to identify QTLs for ovary activation and test the hypothesis that anarchy is recessively inherited. We reject this hypothesis, but identify four QTLs that together explain approximately 25% of the phenotypic variance for ovary activation in our mapping population. They provide the first molecular evidence for the existence of quantitative loci that influence selfish cheating behavior in a social animal.This is an interesting paper but that's not the reason for this posting. The real reason is to contrast the actual paper with the press release from the University of Western Ontario (Canada) [Discovery proves 'selfish gene' exists]. Here's the complete press release.
A new discovery by a scientist from The University of Western Ontario provides conclusive evidence to support decades-old evolutionary beliefs about the existence of a so-called selfish gene.So, what's the beef? The problem is that the press release is horribly confusing. In The Selfish Gene Dawkins argues that one can look at evolution from the perspective of the gene and not the organism. The goal of each and every gene, according to Dawkins, is to replicate itself and pass on copies to future generations. Every gene (allele) is selfish in his view. The selfish gene of The Selfish Gene has nothing to do with altruism. At least not directly.
Since renowned British biologist Richard Dawkins ("The God Delusion") introduced the concept of the ‘selfish gene’ in 1976, scientists the world over have hailed the theory as a natural extension to the work of Charles Darwin.
In studying genomes, the word ‘selfish’ does not refer to self-centred behaviour but rather to the blind tendency of genes wanting to continue their existence into the next generation. Ironically, this ‘selfish’ tendency can appear anything but selfish when the gene does move ahead for selfless and even self-sacrificing reasons.
For instance, in the honey bee colony, a complex social breeding system described as a ‘super-organism,’ female worker bees are sterile. The adult queen bee, selected and developed by worker bees, is left to mate with male drones.
Because the ‘selfish’ gene controlling worker sterility has never been isolated by scientists, the understanding of how reproductive altruism can evolve has been entirely theoretical – until now.
Working with Peter Oxley of the University of Sydney in Australia, Western biology professor Graham Thompson has, for the first time, isolated a region on the honey bee genome that houses this ‘selfish’ gene in female workers bees.
“We don’t know exactly which gene it is, but we’re getting close.”
“This basically provides a validation for a huge body of socio-biology,” says Thompson, who adds the completion of Honey Bee Genome Project in 2006 was crucial to this discovery.
Now, according to the Dawkins' view of evolution, worker sterility is not a violation of the selfish gene principle. Dawkins believes that Hamilton is correct and that altruistic behavior can be explained as an indirect way of propagating one's genes to future generations. Thus, the bee gene is a selfish gene in the Dawkins sense, but so is every other gene (allele) in the bee genome.
This study is not "conclusive evidence" of selfish genes. We've had that kind of conclusive evidence ever since the discovery of alleles that confer fitness advantage—alleles such as those for antibiotic resistance gene in bacteria. This study is interesting because it points to the discovery of altruistic genes (alleles) but that something quite different from what it says in the press release. The "cheater" allele represents selfishness of a different kind.
Incidentally, there's nothing in paper itself about "selfish genes" or Richard Dawkins.
If you want to follow up on this topic you should read the comments on Richard Dawkins.net [New discovery proves 'selfish gene' exists]. As you might imagine, the readers over there are split between those who hail this as confirmation that Dawkins is vindicated and those who have actually read The Selfish Gene. Many are calling for clarification from Richard Dawkins himself. I hope he responds because this is a perfect opportunity for him to set the record straight.
[Photo Credit: The Telegraph (UK)]
Oxley, P.R., Thompson, G.J., Oldroyd, B.P. (2008) Four QTLs that Influence Worker Sterility in the Honey Bee (Apis Mellifera). Genetics. 2008 Jun 18. [Epub ahead of print]Click here to read [PubMed] [DOI: 10.1534/genetics.108.087270]