The insect we study is a species of Drosophila, which is related
to the ones that we study in genetics lab. This Drosophila
feed on mushrooms. When they're in the mushrooms they get
infected with roundworm parasites. The roundworms
grow inside the flies, sterilize them...
unless the flies carry the bacteria which are called Spiroplasma.
And the Spiroplasma have a big negative impact
on these nematode parasites. What I found: in the 1980's,
when I was studying these Drosophila, these insects,
in the fields, was that virtually all parasitized flies
were completely sterile. The nematodes just grow like mad
ah, the flies are bursting with nematode offspring,
hundreds to thousands of them. But what I found recently
is that a large fraction of the flies that are parasitized
by nematodes are fertile. The nematodes are much, much smaller,
very few nematode offspring inside the flies,
and the nematodes really look sick.
If flies carry the Spiroplasma and by some mechanism,
the Spiroplasma are having a big negative impact on the the nematodes.
Which means the nematodes then cannot sterilize the flies.
The difference between the fertility of Drosophila that we collected in the 1980s
where parasitized flies were almost always completely sterile,
and the situation today, where a lot of the parasitized flies
are fertile, indicates that the Spiroplasma
has increased rapidly in frequency
in our local population in the last 20 years.
So we have a couple of lines of evidence that spread rapidly,
we also see that it seems to be spreading from east to west
across North America, so this is a very rapid change
that's occuring in the Drosophila population.
It's allowing them to become more resistant to these nematode parasites
but as I said before, it does not involve
spread of a beneficial mutation in one of
the genes of the fly. It's an increase in the frequency
of infection by the Spiroplasma symbionts.
So how likely is it that these bacteria could have spread
so rapidly? We have actually calculated how fast
the bacteria could spread through a population based on
the benefit that they confer to the insects.
And what we've seen in the wild is
completely in accordance with the very rapid change in the frequency of
infection by Spiroplasma. So,
the rate at which this change occurred is consistent with all our field data.
What's remarkable, I think, is that we're actually able to see this.
That it actually occurred while we were out there looking at things. So,
it could well be that these sorts of changes are going on
beneath the surface all the time,
and with the modern techniques using molecular
PCR detection of bacteria, could be that
we'll see a lot more examples of rapid change like this.
Adaptation by natural selection, as Darwin formulated,
requires three conditions:
First of all there has to be variation in some trait
within a species, and in the case that we're studying,
the variation is whether or not the insect - the flies - are infected
with Spiroplasma. Secondly, there has to be some sort of a
fitness consequence of the theory. Which means that
individuals differ either in their chance of survival or reproduction.
In our case, flies that carry Spiroplasma,
the bacterium, have greater fertility. They leave more offspring than the
than the flies that don't carry Spiroplasma. Finally, the third criterion for
adaptation by natural selection is that the trait
has to be heritable. Which means there's a tendency
for the trait to be passed on from parents to offspring.
In our case the Spiroplasma are transmitted from infected female flies
through the egg to the offspring.
So even though there's no beneficial mutation
involved in this, what there is, is variation
in Spiroplasma infection. As a result of
it meeting these conditions for adaptation by natural selection,
the frequency for Spiroplasma infection actually increases
in the population, and makes the population more fit to its enviroment.