by Matthew Cobb
The biology of aging is one of the sexiest topics around. If we could work out how and why different animals have different life-spans, maybe we could work out how to extend human life-span. (Whether this is a Good Thing or not from the point of view of the individuals concerned, or the planet, is another issue.)
One of the interesting things about aging is that once you stop reproducing, your genes cannot be ‘seen’ by natural selection. Whatever choices you make – where to eat if you’re an animal, what to eat if you’re a human animal – it cannot have a direct effect on the survival of your genes in the next generation, because you’ve already passed them on.
In most organisms, this is generally irrelevant, as they carry on reproducing until they fall down dead or get eaten, or both. But in humans – or more specifically, in human females living since the rise of civilization – there is ample opportunity for living in a zone where natural selection cannot touch your genes. It’s called life after the menopause.
Although it seems unlikely that in prehistory very many women survived to enjoy this phase of their life (disease and hunger would probably have done for them earlier), finding a selective explanation of the menopause has intrigued evolutionary biologists down the ages.
One simple explanation is that although a woman’s direct fitness cannot be affected after she ceases to reproduce, her inclusive fitness can be altered. Her genes would also be present in her offspring or relatives, and they may well benefit from her being around, even though she is not able to reproduce.
The presence of old women (and men) may have been a great advantage to early human societies by enabling human groups to deal with rare challenges in the environment (what to do when drought comes, which rare mushrooms you can and can’t eat), because they remembered what happened years before.
Mosquitoes don’t live in societies, and don’t – as far as we are aware – have any kind of culture. They do reproduce like mad, though, and they are the subject of intense selection pressures as people try to kill them using pesticides, to prevent malaria transmission.
The result is inevitable – the population of mosquitoes evolves resistance. It only takes one fertilized female to show a slight resistance to a given insecticide for that character to sweep through the population, as shown in the figure below, which shows the rapid evolution of resistance in a population of mosquitoes in southern Mexico three years after the introduction of indoor spraying:
In an article that has just appeared in the Open Access journal PLoS Biology (‘Open Access’ means it is free to read for everyone), researchers from Penn State University and the Open University, UK, suggest that this evolution of insecticide resistance could be avoided if the mosquitoes were killed after they had reproduced. In other words, at a period of their life when natural selection couldn’t ‘see’ them.
This idea is not as far-fetched as it might seem – in general the mosquitoes that bite and transmit malaria are the older females, who have already laid their eggs. As the authors put it “Thus, in principle at least, public health advances can be achieved with minimal selection for resistance by an insecticide that kills after the majority of mosquito reproduction has occurred but before malaria parasites are infectious.”
So how do they propose to blindside the mosquitoes and get round natural selection? They put forward several ideas, from slowly-accumulating pesticides to fungal infections that would gradually kill the mosquitoes, hitting the most lethal phase just as they begin to bite.
This cunning plan combines evolutionary insights, a profound knowledge of mosquito/malaria biology and some great lateral thinking. If it can be realized, we will be able to treat mosquito populations with insecticides without natural selection getting in the way.
Citation (from whence the figure above is taken):
Read AF, Lynch PA, Thomas MB (2009) How to Make Evolution-Proof Insecticides for Malaria Control. PLoS Biol 7(4): e1000058
For the full article, go here: doi:10.1371/journal.pbio.1000058