Hunting Elephant Hunters with Robots 1

NS 2810: Unnatural selection: How humans are driving evolution (series)
http://www.newscientist.com/article/mg21028101.800-unnatural-selection-how-humans-are-driving-evolution.html et
seq.



Humans are not only causing a mass extinction--we are also the
biggest force in the evolution of the species that will survive


Hunting down elephants' tusks

Most predators target the young or the weak. Humans are different because we hunt the biggest
and best animals. Those animals with large antlers or tusks are ones that humans like to kill.
Combine this with human's ability to kill in great numbers and the result is extremely rapid
evolution of our prey.

The first clear evidence was published in 1942, and since then many
examples have emerged of how hunting can transform the hunted. The
targeting of large animals has resulted in a fall in the average
size of caribou in some areas, for instance, while trophy hunting
has led to bighorn sheep in Canada and mouflon in France evolving
smaller horns.

Perhaps the most dramatic example is the shrinking of tusks in
elephants, or even their complete loss. In eastern Zambia, the
proportion of tuskless female elephants shot up from 10 per cent in
1969 to nearly 40 per cent in 1989 as a result of poaching (African
Journal of Ecology, vol 33, p 230). Less dramatic rises in
tusklessness have been reported in many other parts of Africa, with
some bull elephants losing tusks too.

Humans have had an even bigger impact in Asia. Only male Asian
elephants have tusks, and the proportion of tuskless bulls has
soared in many areas. In Sri Lanka, where there has been a lot of
poaching, under 5 per cent of males now have tusks, says Raman
Sukumar of the Indian Institute of Science in Bangalore, who studies
Asian elephants. Simulations by Ralph Tiedemann of the University of
Potsdam in Germany and colleagues suggest that female elephants'
preference for tuskers has partly counteracted the effect of
hunting. However, even if all poaching stopped, it would take a very
long time for the percentage of tuskers to rise again.

It's not just animals that are being shaped by human preferences:
the harvesting of wild plants can have a similar effect to hunting
and fishing. In Tibet, for example, the height of the snow lotus at
flowering has nearly halved over the past century as a result of the
flowers being picked for use in traditional medicine (Proceedings of
the National Academy of Sciences, vol 102, p 10218).

To even the balance, some biologists are now promoting the idea of
counteracting the evolutionary pressures of hunting through
"compensatory culling"--killing animals with undesirable traits.
This has actually long been done in some places. In Germany and
Poland, for instance, there is a tradition of shooting yearling deer
with poor antlers to prevent a decrease in the antler size of mature
stags.

Private reserves in countries such as Zimbabwe have a similar
policy. They typically charge hunters a smaller "trophy fee" for
shooting tuskless elephants--$3000 versus at least $12,500 for a
tusker, for example. This is partly because tuskless animals are
less valuable, but it is also a deliberate attempt to eliminate the
trait.
---
The race against climate change

In Finland, the tawny owl used to be mainly grey. But since the
1960s, the proportion of a brown subtype has risen fast. "The
frequency averaged around 12 per cent in the early 60s and has
increased steadily to over 40 per cent nationwide," says Patrik
Karell of the University of Helsinki, whose findings were published
earlier this year (Nature Communications, DOI: 10.1038/ncomms1213).

His team found that grey owls (pictured above right) have an
advantage over brown ones only when there is lots of snow. As
winters have become milder, the brown subtype has thrived. It is
possible that this is because brown owls are better camouflaged when
there is less snow, but it could also be because brown coloration is
linked to another characteristic, such as higher energy needs.

There are countless examples of how global warming is affecting
life, from plants flowering earlier in spring, to species spreading
to areas that were once too cold for them to survive, to birds
becoming smaller. The vast majority of these changes are not genetic
but due to plasticity: organisms' built-in ability to change their
bodies and behaviour in response to whatever the environment throws
at them. At least a few species, however, like the owls of Finland,
are already changing genetically--evolving--in response to climate
change.

In North America, for instance, pitcher plant mosquitoes lay their
eggs in pitcher plants and the larvae enter a state of dormancy in
the winter months before resuming development in spring. Dormancy is
genetically programmed, triggered not by falling temperature but by
the shortening days. As the growing season has lengthened, mutant
mosquitoes that keep feeding and growing for longer have thrived.
Northern populations now go dormant more than a week later than in
1972, when studies began.

The earlier breeding of red squirrels in North America is also
thought to be partly a result of genetic changes. Some families
emerge earlier in spring, and they are doing better as the climate
shifts.

Plants are changing too. When seed collected from field mustard
plants (Brassica rapa) in California in 1997 and 2004 were grown in
identical conditions, the 2004 strains flowered 9 days earlier on
average (Proceedings of the National Academy of Sciences, vol 104, p
1278). The change was a result of drought--the plants have evolved
to reproduce before they run out of water.

Rapid evolution is thus already helping some species adapt to a
warming world, but it is no "Get out of jail free" card. For
instance, so far pied flycatchers in the UK seem unable to shift to
laying eggs earlier in spring. And according to one model that
specifically takes rapid evolution into account, global warming will
kill off 20 per cent of all lizard species by 2080. The problem for
lizards is that as the climate warms, they have to spend more time
in the shade and less time feeding.

Organisms with long generation times and slow reproductive rates are
the least able to evolve, says Stephen Palumbi at Stanford
University. "And they are the ones that are already threatened. It's
a double whammy."

Even species whose evolution has kept pace with the slight warming
so far will not necessarily keep up as the global temperature soars
by another 4 °C or more. Rapid evolution generally depends on the
existing variation within a population, rather than on new
mutations. "It is limited to the kind of changes that can happen
quickly," Palumbi says.

In fact, there is a catch-22 to very rapid evolution--the faster
organisms evolve, the less able they are to evolve further. This is
because fast change occurs when only a small proportion of each
generation manages to reproduce, resulting in a dramatic loss of
genetic diversity--the fuel for further evolution. In many cases,
the size of populations will also plummet, rendering them vulnerable
to extinction. "You could evolve really fast but just not make it,"
says Michael Kinnison of the University of Maine in Orono.
---
The arms race against pests

Had any strange itchy bites or rashes recently? You might have
fallen victim to bedbugs. The little bloodsuckers are back in a big
way, thanks in part to the fact that, like head lice and human
fleas, they have evolved resistance to many common pesticides.

Whatever their drawbacks, there is no doubt that pesticides have
made a huge difference to our lives. They have helped eliminate
diseases like malaria from some areas and made possible the switch
to intensive farming. As soon as we started using them, though,
resistance began to evolve.

"Insects that succumb readily to kerosene in the Atlantic states
defy it absolutely in Colorado [and] washes that easily destroy the
San José scale [insect] in California are ridiculously ineffective
in the Atlantic states," wrote entomologist John Smith in 1897--the
first known report of insecticide resistance.

The use of synthetic pesticides like DDT took off in the 1940s.
Resistant houseflies were discovered in 1946. By 1948, resistance
had been reported in 12 insect species. In 1966, James Crow of the
University of Wisconsin-Madison reported that the count had exceeded
165 species. "No more convincing examples of Darwinian evolution
could be found than those provided by the development of resistance
in one species after another," he noted at the time.

It's not just bugs. Rats and mice around the world have become
resistant to the poison warfarin, and in Europe some have even
become resistant to warfarin's replacement, superwarfarin (Journal
of Toxicological Studies, vol 33, p 283). In Australia, meanwhile,
rabbits are becoming resistant to the poison used to control their
numbers, called Compound 1080.

Because of its economic importance, pesticide resistance has been
studied far more closely than other kinds of ongoing evolution. In
many cases we know which mutations are involved, how they make
organisms resistant and sometimes even how the mutations spread
through populations.

Resistance often arises due to mutations that alter the shape of
proteins and thus prevent insecticides binding to their targets. For
instance, DDT and pyrethroid compounds kill insects by opening
sodium ion channels in nerve cells, but in the malaria-carrying
mosquito Anopheles gambiae, variants of the channels that cannot be
opened this way have evolved on at least four separate occasions
(PLoS One, vol 2, p e1243).

The other main mechanism of resistance involves enzymes that
inactivate pesticides before they can kill. Some resistant strains
of A. gambiae, for instance, produce large quantities of an enzyme
called CYP6Z1 that can inactivate DDT.

Pesticide resistance is becoming such a serious problem that
strategies for preventing it evolving in the first place are taken
increasingly seriously. One approach is to alternate the type of
pesticide applied, to try to avoid applying sustained selective
pressure in one direction.

At present, though, the pests seem to be evolving faster than we can
develop new pesticides. In one region of Burkina Faso, A. gambiae
has become resistant to all four classes of insecticides used for
malaria control.
---
Introducing invaders

In 1935, the South American cane toad was introduced to Australia to
control pests feeding on sugar cane. The cane fields were not to the
toad's liking, but the rest of the countryside was. The toad has
spread rapidly at the expense of many native species.

The highly poisonous animals are having a big effect on predators.
Some, such as the Australian black snake, are developing resistance
to cane toad toxins. Others, such as the red-bellied black snake and
green tree snake, are changing in a more surprising way--their
mouths are getting smaller. The reason is simple: snakes with big
mouths can eat large toads that contain enough toxin to kill them.

The toads themselves are also changing. Some are now colonising
regions that were too hot for the founder population, suggesting
that they are evolving tolerance to more extreme conditions. What's
more, the toads leading the invasion are becoming better colonisers:
they have bigger front legs and stronger back legs than toads living
in the areas already colonised. Radio tagging has confirmed that
these "super-invader" toads can travel faster, as you might expect.
They are probably evolving because the first toads to reach new
areas benefit from more food and less competition, and thus have
more offspring. The changes are likely to be transient, though -
once the toads stop spreading, the "super-invader" traits will
gradually be lost.

Ships and planes have turned the natural trickle of species
spreading to new islands or continents into a raging torrent, and
the new arrivals sometimes have a dramatic effect. In areas of the
US that have been invaded by fire ants, for instance, native fence
lizards have evolved longer legs. They need them: given the
opportunity, a dozen fire ants can kill a lizard in minutes.

Rather than simply study the results of invasions, Michael Kinnison
of the University of Maine in Orono and colleagues have been
actively experimenting. In one experiment, his team moved juvenile
chinook salmon from one river in New Zealand to another. The salmon
were introduced to the country around a century ago, and Kinnison
wanted to assess the extent to which they had adapted to conditions
in individual rivers. He found drastic differences in survival, even
though the fish appear identical (Canadian Journal of Fisheries and
Aquatic Sciences, vol 60, p 1). "When a population was locally
adapted, it performed twice as well," he says.

Kinnison suspects that lots of small changes can add up to make a
huge difference to a population's success. "Contemporary evolution
may be relatively modest on a trait-by-trait basis, but its overall
contribution to the performance of populations may be immense," he
says.

Such findings help explain why there is often a lag between the
introduction of new species and their rapid spread. A newly arrived
species is likely to find itself in an environment that is not quite
ideal, and its population may be very small, meaning there is little
genetic diversity. In these circumstances, a species will spread
only slowly, if at all.

As the population begins to adapt to local conditions, though -
perhaps via invisible changes such as mutations in immune genes--it
is likely to start to grow and spread. Because more mutations occur
in larger populations, it will then evolve faster, enabling it to
spread quicker and further. If this turns out to be common, it is
bad news. It suggests that many introduced species that seem to be
behaving themselves could yet start spreading explosively and cause
serious problems.
---
Living with pollution

Between 1947 and 1976, two factories released half a billion
kilograms of chemicals called polychlorinated biphenyls (PCBs) into
the Hudson river, in the north-east US. The effects on wildlife
weren't studied at the time, but today some species seem to be
thriving despite levels of PCBs, many of which are toxic, remaining
high.

At least one species, the Atlantic tomcod--an ordinary-looking fish
about 10 centimetres long--has evolved resistance. "We could blast
them with PCBs and dioxins with no effect," says Isaac Wirgin of New
York University School of Medicine.

Many of the ill effects of PCBs and dioxins are caused by them
binding to a protein called the hydrocarbon receptor (Science, vol
331, p 1322). The Hudson tomcod all have a mutation in the receptor
that stops PCBs binding to it, Wirgin and colleagues reported
earlier this year. The mutation is present in other tomcod
populations too, Wirgin says, but at low levels.

The most famous example of evolution in action was a response to
pollution: as the industrial revolution got under way,
cream-coloured peppered moths in northern Britain turned black to
stay hidden on trees stained by soot. As the tomcod shows, though,
most evolutionary changes in response to pollution are invisible.

The spoil heaps of many old mines, for instance, are covered in
plants that appear normal, but are in fact growing in soil
containing high levels of metals such as copper, zinc, lead and
arsenic that would be toxic to most specimens of these and other
species. The evolution of tolerance has occurred extremely rapidly
in some cases, sometimes within just a few years of the soil being
contaminated.

With very widespread pollutants, it is much harder to show that
organisms are evolving in response, because all populations change
at once. The comparison has been done with a common weed called
plantain (Plantago major), though. Ground-level ozone, produced when
sunlight strikes car exhaust fumes, greatly impairs the growth of
plants. When researchers grew plantain seeds collected in 1985 and
1991 from a site in northern England where ozone pollution reached
very high levels in 1989 and 1990, they found that the plants from
the 1985 batch grew nearly a third more slowly when exposed to
ozone, whereas the growth of those from 1991 fell by only a tenth
(New Phytologist, vol 131, p 337).

Since even the remotest parts of the planet are now polluted in one
way or another, it is likely that many plants and animal populations
have evolved some degree of tolerance, even though few cases have
been documented. "Nobody looks for resistance," says Wirgin. "My
guess is that if you look you will find a lot of it." His own
discovery was entirely accidental: the team had set out to study
liver cancers, and they only noticed the tomcod's resistance when
blasting the fish with PCBs failed to produce any tumours.

However, there are obviously limits to what evolution can achieve.
This is especially true for small populations that reproduce slowly
and have few offspring, such as the Yangtze river dolphin. Pollution
is thought to have contributed to its extinction.

What's more, pollution resistance in one species can have unexpected
consequences for others. The tomcod's tolerance allows it to
accumulate extraordinarily high levels of PCBs in its body, for
instance, which are a threat to animals higher up the food chain -
such as humans with a taste for these reportedly delicious fish.
---
Spreading sickness

Perch in Lake Windermere in the UK used to live to a ripe old age.
While the average age of fish caught and released by researchers was
around 5 years, a few individuals were as old as 20. Then in 1976,
an unidentified disease wiped out 99 per cent of adult fish and
continued to preferentially kill older fish for years afterwards.
Since then, no fish older than 7 have been caught.

According to Jan Ohlberger of the University of Oslo, Norway, the
perch (Perca fluviatilis) evolved very quickly in response. They now
become sexually mature at an earlier age, which increases their
chances of breeding before they get killed by the disease
(Proceedings of the Royal Society B, vol 278, p 35).

While the disease is thought to have spread naturally in the lake,
Ohlberger points out that many devastating disease outbreaks in
plants and animals are a result of human activity. To mention just a
few: Dutch elm disease was caused by fungi introduced from Asia;
lions were hard hit by canine distemper spread by village dogs, and
corals are far more susceptible to diseases when water temperatures
are abnormally high, which is happening often as a result of climate
change.

Anything that kills a significant proportion of a population has the
potential to bring about very fast evolution. In frogs there is now
some evidence of this: last year several research groups reported
that some populations appear to be becoming resistant to a fungus
that has decimated many amphibian species. It is also clear that
human populations have sometimes evolved rapidly in response to
diseases such as kuru, which attacks the nervous system.

So it seems plausible that by spreading diseases or creating the
conditions in which they thrive, humans are indirectly forcing many
organisms to evolve. "I think this is a common phenomenon and has
not yet been described because it is simply hard to prove," says
Ohlberger. He points out that the long-running capture-and-release
programme at Lake Windermere, which began in 1943 and just happened
to coincide with the disease outbreak in perch, is pretty unique. In
most cases we know too little about what populations were like
before disease outbreaks to be able to tell if and how they have
evolved in response.

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