On the 12th of July, the BBC website carried the article Butterfly shows evolution at work. This brief media report describes the work of Sylvain Charlat (University College, London) and his co-workers on parasitic infection in the tropical Blue Moon butterfly (Hypolimnus bolina).

Blue Moon butterflies are very common throughout the Southern Hemisphere and the South Pacific in particular. Most butterflies, however, are infected with parasitic bacteria called Wolbachia. These bacteria inhabit the egg cytoplasm of the insect and are passed on by maternal transmission from generation to generation. The presence of the bacteria, however, does not appear to disrupt the reproduction of the infected butterflies. In particular, we now know that there is a gene which produces an effect preventing the bacteria from destroying its host. What this suppressor gene actually does and what it might produce is currently unknown.

Unfortunately, however, on some Polynesian islands in the South Pacific, there was a problem. The parasitic bacteria were killing the male butterflies. This phenomenon was described by Sylvain Charlat and his group in the 2005 paper published in Molecular Ecology. In this paper, the authors reported that 6 of the 12 Polynesian butterfly populations studied showed a dramatic reduction in the number of male butterflies. In contrast, however, the bacteria did not kill males in any of the three Southeast Asian populations studied, despite the very high bacterial prevalence there. Presumably, this is the normal situation right across the Southern Hemisphere where the Blue Moon Butterfly thrives happily in the presence of the bacteria.

So what was happening in these isolated island communities? One explanation is that the “suppressor gene” which facilitates happy co-habitation between butterfly and bacteria had been damaged by mutation. As a general rule, mutation leads to the loss of genetic information and a reduction of biochemical efficiency. If this gene were to be located on the female sex chromosome(s), female butterflies would tolerate (and carry) this mutation provided they had other normal copies of the gene. On the other hand, if males only had damaged copies, the bacteria would kill the host, which is definitely not in the best interests of either the bacteria or the butterfly.

This situation might be analogous to any human X-linked genetic disorder. For example, haemophilia results from a faulty gene leading to the production of Factor 8, an essential clotting factor. Males only have one copy of this gene and if it is damaged, then haemophilia results. In the case of the Blue Moon butterfly, however, the situation is much more complex because here we are considering the natural interaction between a bacteria and its host living in symbiotic relationship.

We now know that the presence of a fully functioning suppressor gene is a dominant trait. In other words, if it is present, then the gene product will confer ‘resistance’ to the bacteria’s innate ability to destroy its host. This has been unequivocally demonstrated by the Charlat group and is described in a later publication in PLoS in September 2006.

The restoration of male killing suppression inevitably follows the re-introduction of the healthy gene back into the gene pool of the Blue Moon Butterfly. This is, unsurprisingly, a very rapid process. It is recognizable within one generation and the process is completed with two or three generations.

It is worth noting, however, that the title of the 2006 paper is “Evolution of Male-Killer Suppression in a Natural Population”. Why should this be the case? The assumptions that are made that lead to this title are: (1) that the “original” relationship between bacteria and butterfly inevitably led to the killing of male butterflies (i.e. the norm rather than the exception); and (2) that the acquisition of host suppression of bacterial male-killing ability is an evolutionary process rather than the absence of a genetically inherited disorder.

We maintain that there could be an alternative explanation that would concur with overwhelming evidence. The general rule (reflected in the widespread symbiotic infection of butterfly with bacteria) is that the normal suppressor gene is fully functioning. However, there can be a relatively rare mutation (i.e. once in a blue moon) that leads to the incidence of a genetically inherited disorder that reduces the efficiency of the suppressor. If the male butterfly only has damaged copies of this gene, it would inevitably become vulnerable to the bacterial ability to kill its host – literally, given half a chance.

Is this another example of misplaced enthusiasm for the Darwinian process? Truth in Science looks forward to future publications of this extremely interesting phenomenon.