We’ve spent some time on the big bee die off (although not on the mobile phones) as have many other blogs and newspaper articles. In the US, the problem has reached epidemic proportions and has raised serious concerns about the future of several crops that depend to a large degree on bee pollination. Unfortunately recent evidence seems to suggest that the problem, which has been called Colony Collapse Disorder (CCD) has been spotted in Europe, as well. The cause or causes of CCD are unknown, but the list includes the usual suspects ranging from transgenic crops and pathogens to global warming and newly developed pesticides. Oh yes, and cell phones.
So the e-publication of a paper due to appear in the Journal of Heredity ((Variation and Heritability in Immune Gene Expression by Diseased Honeybees. Laura I. Decanini, Anita M. Collins, and Jay D. Evans Journal of Heredity Advance Access published online on April 2, 2007, doi:10.1093/jhered/esm008)) (behind a paywall) is timely. It describes the heritability and genetic variation of a gene called abaecin which is a key component of the immune system of bees.
Bees, like nearly all eukaryotes, have an innate immunity, but are generally thought to lack the additional adaptive immune response, which we and most other vertebrate species have. That is to say insects can’t get the ‘flu and respond by making specific antibodies to the virus (In fairness, the notion that insects do not have an adaptive immune system has been challenged recently by studies in Drosophila. ((Extensive Diversity of Ig-Superfamily Proteins in the Immune System of Insects Fiona L. Watson, Roland Püttmann-Holgado, Franziska Thomas, David L. Lamar, Michael Hughes, Masahiro Kondo, Vivienne I. Rebel, Dietmar Schmucker. Science Vol. 309, pp. 1874 – 1878 DOI: 10.1126/science.1116887 Abstract here.)) )
To find out whether abacein expression differed between bee populations, scientists at the US Department of Agriculture crossed several unrelated males into a homogeneous maternal background and then challenged the offspring with Paenibacillus larvae. This is the bacterium that causes American foulbrood, a widespread larval disease of bees. Subsequent measurements in affected larvae showed that the level of abaecin was moderately heritable but highly variable, differing by as much as 10,000 times between different lines. Why this is variation exists at all is a matter of speculation, but it might be due to selective pressures: an arms race between hosts and different pathogen strains or species.
At any rate an understanding of the components of the immune response in bees at the molecular level and the realization that there appears to exist considerable genetic variation that could be exploited would seem to offer one of the more promising approaches to selection for pathogen resistance. Whether that will stop CCD is anyone’s guess ((From Michael Kubisch)).