Do Bald Men get all the Girls ?

That is science, not science fiction. Research has revealed that bald males command a more substantial harem of females than their hairier counterparts...which is, in the event the bald male is really a maneless Tsavo lion from Kenya. In humans, hair loss (or androgenic alopecia) continues to be associated with numerous biological pathways.

I will simply target the best publicised cause, an over-responsiveness to DHT, or dihydrotestosterone for many who enjoy long words. This hypersensitivity are closely related to some variety of factors. As an example, high quantity of a receptor for DHT on follicles of hair, or even a characteristic and much more sensitive structure from the receptor in predisposed people, could cause the head of hair follicle to detect more DHT than is wonderful for it. In fact, one proposal for why hair is lost in the particular pattern (hence the word hair loss) happens because follicles of hair within the parts of typical hair thinning normally express higher amount receptor. Chief on the list of culprits though, a minimum of based on current thought, can be an overproduction of DHT. The enzyme 5-alpha reductase converts testosterone into DHT. In people predisposed to baldness, the degree of the enzyme is frequently raised inside the scalp and skin, causing a higher concentration of DHT that will affix to the receptors on follicles of hair. On the other hand, for those who have average amounts of 5-alpha reductase but high amounts of testosterone, it might be also possible to obtain additional than the usual healthy balance of DHT, but this hypothesis is sort of more controversial. İn support of the idea, even though the pattern will look slightly different, women may also exhibit hair loss. Normally, oestrogen counteracts the consequences of testosterone, but after menopause a ladies oestrogen level falls and her testosterone (yes, women produce this 'male' hormone too) is now able to changed into DHT and cause baldness.

DHT is considered to promote hair thinning in three ways:

1. Healthy follicles grow hair for a while, usually for 2-5 years, after which come out before beginning to develop hair again. DHT shortens the head of hair growth serious amounts of raises the follicle's hair regrowth holiday. This leads to fewer new hairs and shorter ones at this.

2. Immediately before a wholesome follicle stops new hair growth, it shrinks and also the hair it creates is thin and weak (vellus hair). DHT causes the follicle to contract prematurely which explains why bald folks have peach fuzz on the heads.

3. Follicles require a circulation being nourished. DHT could cause less blood to flow towards the follicles.

Bald Lions

Where do the Tsavo lions can be found in? Unlike balding men, Tsavo lions usually do not lose their pre-existing hair - their manes never grow. Nonetheless, it's been suggested they are susceptible to something comparable to male-pattern baldness his or her manelessness might be due to elevated amounts of testosterone. That is merely a hypothesis; area of work testing hormonal changes of the lions recently been started earlier. However, maneless Tsavo lions use a track record of being extremely aggressive, a trait associated with high testosterone. If they certainly have an overabundance testosterone compared to the average African lion it appears reasonable to declare that much more of hormone agent is changed into DHT, which stops their manes from growing because of the three biological actions in the above list. It is very important to keep in mind though that is probably not explanation for their baldness. Even though their testosterone levels are high, there could be various other important genetic causes of the absence of manes. Male Tsavo lions are now living in two kinds of social groupings: Adults roam because the sole male among an extremely large numbers of females in the group termed as a 'pride'. İt is really an unusual social structure for lions as there are usually a minimum of two males atlanta divorce attorneys pride. Another bizarre social feature of those lions is the fact that nomadic males stick together. This is thought-provoking, particularly if it really is realised that males inside a pride actively do not let other males to become listed on. Why would some lions not tolerate other males while some seek their companionship? The theory is the fact that they are coalitions of adolescent males that hunt together, but once their testosterone levels peak, they become too competitive as well as the group splits up.

Bald along with a social outcast, or even a sex magnet?

Set up attitude could possibly be proven accurate statistically, there's a common conception available that human females find bald men less attractive. Adult Tsavo lions don't appear to own this problem though. Besides one guy get All of the girls, but he gets more girls compared to the other African lions with hair would even when these were the only real male inside their pride. So, is that this social construct a lady choice or perhaps a male choice? Do the females decide to cluster across the bald male, truly making the group a 'male pride' or may be the bald male forced to reside only among females because there could be an excessive amount of competition amongst other adult men? Unless we learn how to speak Lion Lingo and question the lions directly, I suppose we are going to can't predict the solution to that question with absolute certainty. I am no zoologist, therefore it is feasible for testosterone levels have absolutely nothing related to social groupings, or manelessness, among Tsavo lions and it's also only a peculiarity with this group.

But imagine if the social grouping of bald animals did have connected with testosterone... Perhaps whether it we looked at it more closely, we might find such like in humans. Perhaps men whose hair thinning comes from other non-hormonal causes are really less appealing to women because, well, females like hair. In essence, only cosmetic squeamishness. And maybe men whose baldness is hormonal tend to be more successful with all the ladies since they distribute invisible signals (pheromones) in charge of chemical attraction. Or maybe they don't really go along well with males with clashing hormonal profiles and also have were required to figure out how to understand women better instead. Naturally, this really is all speculation on my part, nonetheless it enables you to wonder what lions from some remote world might teach us about ourselves and our dispositions!

Deadly Cone Snails (Conus) Harbour Painkillers of the Future

"I seem to have been only like a boy playing on the seashore, and diverting myself in now and then finding a smoother pebble or a prettier shell than ordinary, whilst the great ocean of truth lay all undiscovered before me." Sir Isaac Newton (1642-1727)

Snails. Yes, I know, it's hard to get excited. You think snail, you think, slime. You think slow, squidgy, meandering ball of wibbly-gloop. With eyes on stalks. Then again, you might just think of garlic. Snails are pathetic English garden munchers!

Or are they? Not all snails are born equal. Some snails are born with heightened killer instincts, roaming beneath the ocean's surface, waiting, hunting for that one precious meal. And we're not talking limp lettuce - some snails are content with nothing less than bagging an entire fish! And should you, my friend, be unlucky enough to disturb one of these molluscs whilst out having a leisurely paddle, you could be well on your way to the great paddling pool in the sky.

Great White sharks are passé, welcome to the world of the genus, Conus…

Collecting beautifully patterned Conus snails off the north east coast of Australia might sound like hard work, but it's not all boats, sun, fresh air and sea. Dr Bruce Livett of Melbourne University takes it all in his stride, though. For nearly a decade, he and his team of enthusiastic colleagues, students and friends have sought and studied these spectacular snails.

But why is a neuroscientist interested in these animals? Because, apart from their spectacularly patterned shells, these molluscs have a secret weapon - one that may revolutionise the treatment of pain. A typical poisonous snake might unleash a couple of different nerve toxins on its furry victim; but what the Conus lacks in speed, it more than makes up for in poison. These snails are positively brimming with nasties, often shoving around 50 individual toxic mini-proteins into their victim.

Your brain, under normal circumstances, is a finely honed thinking machine. The reason being that all of its nerves are able to function correctly, sending messages, receiving messages, processing the information and giving a pretty good output. If the brain is like an organic computer, then being stung by a Conus is a bit like pouring a pint of ale on a laptop. Fizz, bang, splutter, dead.

The reason is that each of the tiny proteins that make up the toxic cocktail are targeted at different parts of the nervous system: these snails don't just 'blow the bloody doors off' your brain, they terminate it from every conceivable angle!

But not all the components in the venom are deadly. Some turn out to be good for you. As they say "no pain, no gain". So what about the future of pain? Painkiller research can be riddled with problems: side-effects, dependency, efficacy. What about a painkiller that is as effective as morphine but has no apparent side-effects? The relatively few humans who have witnessed a death-by-snail have noted the absence of pain. And Bruce Livett and his team now know why.

One of the toxins in the sting of the Conus victoriae species, is a string of just 16 amino acids (the Lego units that make proteins). This tiny protein, ACV1, binds to bits of the brain that would normally allow us to feel pain, and shuts them down. What we potentially have here is a powerful new generation of analgesics. This new 'drug' has done very well in pre-clinical trials and is now undergoing toxicity tests prior to entering clinical trials, the rights for development into a drug having been bought by a company called Metabolic Pharmaceuticals.

So, spare a thought for our British, plant bound relatives. Maybe they deserve a little more respect. After all, with relatives like the Conus, you don't need to be pretty.

"It is perhaps a more fortunate destiny to have a taste for collecting shells than to be born a millionaire."
Robert Louis Stevenson (1850-1894)

Barry Gibb

Human Cloning, Part 2 - The Process of Animal Cloning

In the first part of this mini-series we looked at the earliest stages of mammalian development, from the egg and sperm to the ball-like blastocyst. In this second part we turn to the story of cloning, and the technical problems and limitations of the process.

Although cloning burst onto the global media scene with the arrival of Dolly the sheep in 1997, the technology has been around for decades. At its most basic the process involves taking an egg cell and replacing its chromosomes (DNA) with the DNA from another cell, and kick-starting the 'developmental programme' with chemicals, or an electric pulse (figure 1). This process is known as Somatic Cell Nuclear Transfer, or SCNT for short. Hans Spemann first proposed such a "fantastical experiment" in 1938, and in 1952 tadpoles were cloned from embryonic frog cells. John Gurdon first successfully cloned frogs from differentiated (developed) cells in 1962 and since then the full list of successfully cloned animals has expanded to include also mice, cows, rabbits, pigs, sheep, cats, horses, zebra fish and monkeys.

1. Cloning requires an egg cell, and an adult donor cell. The (unwanted) chromosomes are removed from the egg cell and discarded. The nucleus, containing the DNA to be cloned, is removed from the donor cell.		2. The donor nucleus is inserted into the empty egg cell, a process called somatic cell nuclear transfer (SCNT). Afterwards the egg contains a full (adult) set of chromosomes as if it had been fertilised normally.		3. A pulse of electricity, or a chemical 'shock', kick-starts the development process, and the embryo begins to grow.		4. Cell division begins. The subsequent development of the embryo depends upon how successfully the donor nucleus has 're-programmed' the egg.
Figure 1 - The process of embryonic cloning

However, not all clones are created with equal ease. Cloning success is much more likely if embryonic cells are used as nuclear donors. These could be embryonic cells taken from an early fetus, or cells from the inner cell mass of the blastocyst (see Cloning Part 1). What made Dolly so special was the fact she was the first mammal to be cloned using a cell taken from an adult - and even then she was the only live animal to be born out of nearly three hundred attempts. Since then, other animals have been cloned from adult cells, but the efficiency of achieving live births is still extremely low. So what's the big difference between embryonic and adult cells? The key lies in the concept of epigenetics, which was introduced in the first part of this series (see also an earlier article about genetic imprinting).

Cloning requires the reprogramming of an adult or embryonic cell right back to the very start of development. Adult cells are more differentiated (specialised) than embryonic cells - they have made decisions about what sort of cell to be and these choices are said to be imprinted within the cell. For example, an embryonic cell has the potential to become all sorts of cell types, whereas an adult liver cell can only be a liver cell. So embryonic cells only have to "forget" a few decisions when they are cloned, whereas an adult cell has been through many more choices so, essentially, the clock has to be wound back further.

Cells remember what type they are due to epigenetic modifications of their DNA: molecular tags which mark certain genes as being switched on or off. These tags are very similar to those on the sperm which are removed shortly after fertilisation by reprogramming factors in the egg. In order for an adult or embryonic cell to be reprogrammed by cloning (by exposing it to the reprogramming environment of the egg), the epigenetic marks within the DNA must be removed. Adult cells are believed to have more of these tags than embryonic cells, so are harder for the egg to reprogramme.

Whether the donor cell is adult or embryonic, a successful clone must negotiate all the stages of development from one cell to a blastocyst and then on to being a fully-grown baby. But embryos can only be grown outside the womb in a test-tube until the blastocyst stage. After this, the embryo needs to form a placenta and take resources from the mother. Researchers must transfer the little balls of cells into the womb of an appropriate surrogate mother, where it can grow further. In fact, embryos created by mixing eggs and sperm in IVF clinics are usually transferred before the blastocyst stage- often when they only consist of two to eight cells.

Experiments in animals such have mice have shown that there is a high proportion of success in growing cloned embryos up to the blastocyst stage. Even embryos containing twice the normal number of chromosomes can grow quite happily to this point, even though a baby with this many chromosomes could never be born. Yet if these embryos are transferred into surrogate mothers, very few of them produce babies. This is because the egg contains many of the ingredients required for the early stages of development, and will direct the formation of a blastocyst even if there are severe problems with the DNA and chromosomes within the embryo. But to grow from a blastocyst to a baby requires complex patterns of genes being switched on and off. This can only happen if the DNA of the donor nucleus has been fully and correctly reprogrammed by the egg during the first stages of the cloning procedure. So it appears that even if you can create a clone, and even if that clone makes a blastocyst, you are still highly unlikely to end up with a baby.

But all is not lost. Blastocysts are extremely useful even if they don't go on to make a fetus. They are the source of the infamous embryonic stem cells, or ES cells for short. ES cells are made by removing the inner cell mass from the blastocyst and growing it in a dish (figure 2). After a time, a colony of special cells with almost magical properties appears. These cells have the capacity to form any tissue of the body, and can be treated with various chemicals to achieve this. They can also replicate themselves many times, to create large populations of useful cells. Genetic engineering techniques work very well in ES cells, allowing mutant genes to be repaired, and new genes to be added.

1. To make embryonic stem cells (ES Cells), the inner cell mass is removed from a blastocyst.		2. The inner cell mass is transferred to a petri-dish, covered with a nutrient solution, and allowed to grow.		3. The inner cell mass soon develops into a large cell colony which can then be divided into smaller clusters of cells that will themselves continue to grow and multiply.
Figure 2 - How to make Embryonic Stem Cells (ES Cells)

Much weight has been placed on human ES cells as a viable therapy for many diseases such as Alzheimer's and Parkinson's. Although we are far from fully understanding the biology of these mysterious cells, they are certainly brimming with promise. In part three of this series we'll look at the latest developments from South Korea, combining ES cell technology and cloning. Are human clones just around the corner? Or are they already here?

Kat Arney

Human Cloning, Part 1 - Making Babies the Natural Way

Few people can have escaped the newspaper headlines over the past few months. The fertility doctor Panos Zavos claimed to have cloned a human baby, while a team of researchers in South Korea also presented their clones to the world. So what's the difference between these stories? And are we really going to see cloned babies peering out from their prams in the near future? In this first article we will spy on the earliest moments of life: how an egg and sperm make a ball of cells that eventually become a baby. Then we can ask if, and how, these processes can be bypassed by cloning.

The first thing to understand is how babies are made - no sniggering at the back, please! To do this, we need to know a bit about eggs and sperm. Eggs are relatively large cells and contain lots of biological goodies required for early development. They are also rather unusual in that they are frozen in the act of dividing their DNA from a full set of chromosomes to half a set (see figure 1, below). This division is important because the sperm also carries half a set: together they make up a full set in the new baby.

At the moment of fertilisation the sperm enters the egg, and things start getting exciting (at least, in biological terms). The following descriptions show what happens in mouse development: we currently do not know whether human development is exactly the same, but it is likely that many events are similar. When the sperm goes in, it reactivates the division process in the egg, causing the arrested chromosome half-sets to separate. The unwanted chromosomes are booted out and form a little cell called the polar body, with no further part to play in the unfolding developmental drama (see figure 1, below). The remaining egg chromosomes organise into a ball-like structure termed a pronucleus. At the same time, proteins in the egg begin to unpack the sperm DNA, expanding it to form another pronucleus (see figure 1, below).

1. An early egg cell. Humans carry 23 pairs of chromo-somes. We inherit one half of each pair from our mothers, and the other half from our fathers. These half-sets of chromosomes are produced in a special form of cell division called meiosis which produces eggs and sperm.		2. A mature egg. In this egg, for simplicity, only one pair of chromosomes is shown (in pink). The process of cell division remains frozen until the egg is fertilised by a sperm		3. Fertilisation. When a sperm penetrates the egg it kick starts the completion of meiosis. One of each pair of the egg's chromosomes is randomly ejected from the cell to form a structure called a polar body. The remaining chromosomes form the egg pro-nucleus.		4. One cell embryo. The half-sets of chromosomes from the sperm are unpacked to form the sperm pro-nucleus. As each pro-nucleus contains half the normal chromosome number, together they produce a cell with a full complement of genetic material.
Figure 1 - The formation of a mature egg and a single celled embryo.

But strange things happen to the sperm DNA: it is stripped of methylation, a special molecular tag that helps the cell to use its genes properly. In the first few hours of development other dynamic changes happen to the sperm pronucleus, especially alterations in the DNA packing proteins within it. These changes in methylation and packing proteins are termed "epigenetic modifications", as they affect the DNA without actually changing the underlying DNA sequence - only the tags and markers around it. Epigenetic marks are important because they tell the cell which genes to use in different types of cells. This is crucial because all our cells contain essentially the same DNA (and therefore the same genes): it is the different patterns of gene usage that give all our cell types their distinct characteristics. Some epigenetic marks act as silencing signals for genes, while some have an activating effect. For example, in a liver cell, liver-type genes would have activating marks while muscle genes would have silencing marks. Conversely, in a muscle cell the muscle-specific genes have activating tags whereas the liver genes are silenced.

Many epigenetic changes take place while the embryo is still a single cell, and these mainly occur within the sperm pronucleus. These molecular upheavals are essential for reprogramming the sperm, so it can be used correctly in the next steps of development. But the epigenetic adventures don't stop at the one-cell stage. The new embryo divides into two cells, then four, then eight and so on until it is a ball of around a hundred cells (see figure 2). Throughout this flurry of activity, more molecular tags are removed from the DNA while other epigenetic modification patterns are established. Eventually, after 4 to 5 days, the ball of cells begins to take shape. A cavity forms and fills with fluid, pushing the cells outwards until the ball is almost hollow and looks rather like a football. We call this a "blastocyst". But the blastocyst is not quite hollow, because lurking on one side is a small clump of cells, somewhat obviously named the "inner cell mass". It is from this unpromising cluster that we all grew: these are the stem cells of the embryo. It is also clear at this stage that there are distinct epigenetic differences between the outer cells and the inner cell mass.

The 2 pronuclei merge, producing a cell with a complete set of 46 chromosomes (23 pairs), The cell begins to divide, giving rise to 2, then 4, then 8 cells, and so on.		The cells continue to divide, undergoing further epi-genetic changes until they eventually produce a cluster of cells resembling a mulberry, called a morula.		A blastocyst is a hollow cell ball containing a cluster of stem cells (the inner cell mass). The inner cell mass (which gives rise to the baby itself) is epi-genetically distinct from the outer cells, which produce the placenta.
Figure 2 - The development of the early embryo

By this time, the embryo has made it to the uterus (womb). The outer cells of our embryonic football start invading the inner wall of the uterus and eventually make the placenta, the large organ that allows nutrients and waste to be exchanged between the mother and the baby. Meanwhile, the small clump of stem cells start dividing and undergo yet more epigenetic changes. An amazing programme of gene activity starts in these modest cells, causing them to organise and create all the parts of a new life. In the next article we'll find out how how cloning fits in to this natural developmental agenda.

Kat Arney

The Great White Shark

It's late in the afternoon. The water is dark and an especially large amount of plankton reduces the underwater visibility to a minimum. Some time ago it occurred to me that with such poor underwater visibility I could probably forget about the object of my visit, to take underwater photos of the great white shark.

Like many previous occasions, I am sitting at the boat's stern between the two 80 HP outboard engines, the camera levelled. Through the viewfinder I am watching the neoprene seal-dummy which our little boat is pulling behind it on a fishing line. I support my arms on my knees, to ease my tense muscles. In the past I have often had to remain in this position from the early afternoon until sunset, through heavy swell, rain and storms, just to take the picture of my dreams - a breaching white shark, leaping for prey. Until now, all my efforts have been in vain.

Dyer Island is located six nautical miles off the coast of Gansbaai (170 kilometres south-east of Cape Town), on the opposite side of which is the small island known as Geyser Rock which is home to an estimated 60,000 South African Fur Seals. As long as the seals stay ashore, they are safe. But when they leave for the open sea to catch fish, they have to negotiate a dangerous shark-infested channel between the islands called "shark alley" which, not surprisingly, is reputed to the best place in the world to watch white sharks.

The sharks patrol mercilessly here, and there is no way to escape them. The seals run the same gauntlet when they return to the island, and those swimming alone, and very young seals swimming close to the surface, face the greatest threat.

This is the scenario we have attempted to reconstruct in this case, with the hope of luring a white shark to reveal itself to the camera. For hours I have been keeping my lens pointing at Koekie, the artificial neoprene seal bobbing along behind the boat. Suddenly, a huge and very heavy body is rocketing out of the water like a torpedo. It has "Koekie" in its mouth. Everything happens in a split second.

It's a precise attack with a fatally perfect timing. A real seal would not have stood the slightest chance. Every single square centimetre of this exquisite creature is vibrating energy. An unforgettable sight. The incredible dynamic of the leap is captured in the picture.

The cause of this unpredictable and unusual attack seems to be the movement, the form and the size of the prey. Until now, such breaching sharks have only been observed in the False Bay and nowhere else in the world (see Peter Benchley/David Doubilet, Great White, National Geographic April 2000).

The great white shark (Carcharodon carcharias) has been around for at least 3.5 million years, but now it is acutely threatened by extinction. It remains to be seen whether the species is already "genetically extinct" - in other words there are so few individuals left that the survivors are genetically very similar to one another and are less likely to be able to withstand other insults that nature can throw at them. The number of sharks, of all kinds, caught every year is estimated at 100 million. Half of it is 'bycatch', which is thrown away. With this overfishing the shark population is irreparably damaged. Due to the decimation in their numbers, which has lasted for decades, and their low reproduction rate, the prospects for the great white shark do not look good. And even though, since last autumn, it has been internationally protected, supervision of the ban on fishing has not been easy.

But perhaps modern science will be able to help at the last minute - at least in this area. A new, very specific rapid test, which only picks up material from white sharks, is able to prove almost error-free, if there are any parts or remains of white sharks in a sample, which would constitute an infringement of the prohibition. This biochemical test, called Pentaplex PCR test or bi-organelle test, was developed by Prof. Mahmood Shivji of the Nova University in Florida, USA.

Part of the image problem facing sharks is thanks to the movie "Jaws". As one review I came across put it, "Peter Benchley's world bestseller has become a Blockbuster, which changed the untroubled relationship between humans and the sea and its inhabitants forever. The primal fear of the danger from the depths was given a fearsome face". Peter Benchley, the author of "Jaws", has since become one of the world's most prominent shark protectors. His latest book is titled "Shark Trouble. True Stories About Sharks and the Sea".

Sharks play an important role in the ecosystem of the sea and they have always fascinated me. I have been responsible for extensive underwater work in many large harbour construction projects all over the world, usually under conditions of poor underwater visibility. Altogether I have spent almost 13,000 hours underwater. There have always been sharks, but I have never had any problems with them. The dreaded inhabitants of the oceans are anything but man-eaters and aggressive monsters. In reality, very few of the 460 types of sharks discovered so far pose a threat to humans.

My objective is to document the sharks on the 'red list', to make them known to the public at large, and to make people think. The documentation of these animals is very difficult and, unfortunately, extremely time and cost-intensive. But sharks have no lobby and there is not much time left. If we don't move fast enough they face extinction before they have even been researched and documented.

Klaus Jost

Global Warming, an Ecosystem Shift, and Sharks in Alaska

The Kodiak Alaska Department of Fish and Game office door flew open and in tromped two fishermen, one with a loaded shotgun, and both with an attitude. "We need to talk to the biologist" the larger bearded man stepped forward, "the one who closed the shrimppin!" The fishermen told the biologist to "either open the fishery or there would be trouble," and that's when I got the telephone call.

At the time I worked for the Alaska Department of Fish and Game's Commercial Fisheries Division, at the headquarters' office in Juneau. The Kodiak biologist put me on the telephone with the irate fisherman, the one with the gun. "We are just trying to do our job," I exclaimed, but it was difficult to explain the Department's position to a fisherman who needed to fish, needed to work to pay bills, keep the house, and feed the kids, all the things that are important to any father. Nobody got shot that day, and the Kodiak fishermen were restricted from fishing for shrimp and crab, fisheries that had been worth millions of dollars the year before.

Trophic Regime Shift
Closing the crab and shrimp fisheries in the Gulf of Alaska was the only way the Alaska Department of Fish and Game could protect the breeding stock, but populations continued to decline. That was in the late 1970s, and through the early 1980s. Mid-water trawl surveys done from the 1950s through the 1980s showed the shrimp, crab, and forage fish (small, high-fat, schooling fish such as herring and capelin) populations declined dramatically during the mid-1970s (see Figure 1). Additionally, data showed huge increases in other species, especially larger predatory fish like Pacific cod, walleye pollock, halibut, and arrowtooth flounder. In a few years the Northeast Pacific ecosystem had changed, with a new suite of species dominating the northeast Gulf of Alaska. Scientists refer to this change in species composition as a trophic regime shift.

Figure 1 Pictorial evidence of the Northeast Pacific regime shift. The methods and locations for collecting the sample from the mid-water small-mesh trawls were similar from year to year.

At the same time the shellfish population was declining in the Gulf of Alaska, shrimp and crab populations were on the increase in the northwest Atlantic Ocean, off the coast of Newfoundland. As the Earth warms we can expect the Gulf of Alaska water temperature to increase, but the in the waters off Newfoundland the temperature will probably decrease for a time as cooler water from the melting Arctic Ocean ice cap flushes past. The two oceans appear to be connected, but going in opposite directions.

Regime shifts are a change in the marine ecosystem occurring inter-decadally and globally. They are induced by what is referred to as climate forcing, or increases in global temperatures or global warming. As oceans warm, the habitat used by a suite of small plants and animals (phytoplankton and zooplankton) will change, often promoting an entirely different suite of phytoplankton and zooplankton. Certain phytoplankton and zooplankton will promote a benthic (bottom of the ocean) ecosystem, while others appear to promote a pelagic (free living in the water column) ecosystem. Colder waters in the Gulf of Alaska seem to promote the benthic system, and the same is true for the waters off the coast of Newfoundland. Warm waters in the Gulf of Alaska have been favourable to pollock and flatfish, but also to salmon which have had record survival and returns in Alaska since the 1980s.

Beginning in the late 1970s, Alaska researchers observed numerous changes in the Gulf of Alaska ecosystem. Stellar sea lion and harbour seal populations declined, and commercial fishing was allowed for pollock and other groundfish species. The sea lion population declined to the extent that they were listed as an endangered species. To help protect sea lions some areas were closed to fishing.

Sharks
By the 1990s fishermen were starting to report sightings of salmon sharks in the region, and commercial long liners, who fish on the bottom of the ocean for halibut and cod, were catching Pacific sleeper sharks in large numbers. These same fishermen were also losing much of their harvests to feeding sharks that would attack and eat the hooked halibut and cod. A third species of shark, spiny dogfish shark, also became more common. During the 1998 Copper River sockeye salmon fishery, dogfish sharks were so abundant they would often plug up and ruin fishermen's nets.

By 1996, throughout the region, but especially around Kodiak Island, Lower Cook Inlet and Prince William Sound, large salmon sharks were abundant in bays and passages. Indications were a new top predator had established itself in the Northeast Pacific, possibly influencing the ecosystem as sea lions and seals did before the regime shift.

Alaska Shark Assessment Program
I started the Alaska Shark Assessment Program in 1998 to look at historical data and to begin measuring and tagging sharks. The historical data described shark population increases and fluctuations, raising some theories to explain why the sharks are so abundant. The International Pacific Halibut Commission, and Alaska Department of Fish and Game have data that indicate huge increases in the numbers of sleeper and spiny dogfish sharks in the Northeast Pacific. As a result of investigating the historical data, a pilot field shark research project began in Prince William Sound in 1999. The research team was an informal group coming together to observe and understand this boom in shark numbers. The team had researchers from the Conservation Science Institute, National Marine Fisheries Service, Alaska Department of Fish and Game, and the University of Washington.

Salmon Sharks
Salmon sharks (Lamna ditropis) (above right) are warm blooded, large, and reported to be one of the fastest fish in the ocean. Their outward appearance is similar to that of the great white sharks, which are in the same family. Because they are warm blooded, with a core body temperature of about 80 degrees F, salmon sharks are high energy fish with a high metabolism to match. To stay warm, salmon sharks have an elaborate heat exchange system which keeps their brain, eyes, and muscles warm and functioning at full performance. At more than ten feet in length, and weighing over 700 pounds, but without the fur or blubber that insulates sea otters and seals, salmon sharks need to consume large amounts of prey each day to generate heat. They hunt opportunistically for herring, rockfish, halibut, pollock, spiny dogfish, squid, sablefish (black cod), and of course salmon. They are both active and aggressive predators. I have observed them thrashing the water, sometimes leaving the water completely, as they pursue their prey, often in what appears to be cooperative feeding.

Pacific Sleeper Sharks
Pacific sleeper sharks (Somniosus pacificus) (right) are large bottom dwelling predators that can be found at depths of over 2000 feet, and specimens exceeding 20 feet in length have been caught in Alaskan waters. Their list of known prey items includes salmon, pollock, herring, rockfish, halibut, sablefish, shrimp, marine mammals, and even other sharks. We were surprised to find bright pre-spawning salmon in their stomachs, indicating they may in fact be feeding near the surface, probably at night. Over recent years, in some areas, longline fishermen have lost much of their fishing gear and catch to sleeper sharks, forcing them to find other locations to fish.

Spiny Dogfish Sharks
For those of you who have enjoyed fish and chips at your favourite English eatery, you may be surprised to learn you were likely eating spiny dogfish shark (Squalus acanthias). Spiny dogfish get their name from the sharp spines, which are sharp enough to easily pierce my boot and leave a lasting scar, which line their backs, and also from the fact they often travel in packs, like wild dogs might. Dogfish sharks are small, growing to about five feet long, but they make up for this in numbers. Dogfish shark fisheries around the world have targeted this tasty morsel, leading to over-fishing and concern for their populations, although dogfish numbers in Alaska are high in some areas. The dogfish shark appears to locate and utilize patches of prey. This happened during the summer of 1998 when the sharks were feeding on forage fish, eulachon in this case, near the Copper River. The spiny dogfish were so abundant they plugged salmon fishermen's gear, often sinking and destroying nets. Yakutat fishermen sometimes catch so many dogfish sharks they move to other areas or stop fishing. Spiny dogfish also have a varied diet including eulachon, herring, shrimp, crab, rockfish, and pollock.

Shark Behaviour
All of these sharks are long lived. We know very little about their reproductive behaviour, except that, in common with many long-lived animals, the rate is low. The longest gestation period is probably that of the spiny dogfish shark which lasts 22-24 months, exceeding that of elephants and whales. All three of these shark species can be found in the waters of Alaska year round, but the salmon and dogfish sharks are migratory, possibly leaving the Gulf of Alaska waters and returning during the summer.

The shark research efforts are designed to determine feeding habits, numbers and movements of salmon and sleeper sharks. One of the tagged salmon sharks was recaptured 650 miles to the south only 48 days later. We suspect female salmon sharks, migrate to the coastal waters of California to give birth to pups in the warmer waters, a behaviour that they share with whales which also often move to warmer water to give birth. We also deployed tags that collect depth, temperature and location data, disengage from the shark at a preset time, and relay their data to satellites. This information has been useful in understanding shark behaviours which may help us understand their importance and influences on the marine ecosystem.

During the field work we were accompanied by National Geographic Society Television, and the British Broadcasting Corporation (BBC) television crews. BBC was filming for their series on the oceans and had especially good shark filming opportunities in Prince William Sound. National Geographic Society deployed their CritterCam which is strapped to a salmon shark's dorsal fin and operates underwater as the shark swims about. At a preset time the camera releases from the shark and floats to the surface where it is collected. Some of this film footage may appear on television.

The salmon sharks we caught were big, with mouths full of teeth, and weighed upwards of 400 pounds. It was sometimes difficult to control the fish on board while taking measurements and attaching tags and the CritterCam. In order to protect the fish from injuring itself we moved the shark into a crib, covered their eyes with a damp cloth, and placed a hose in their mouth to keep seawater flowing over their gills (right).

Salmon sharks (right and above) are at the top of food web and therefore have few predators, although I noticed scrapes and puncture wounds on many of them which are probably the results of encounters with killer whales (left) which prey on salmon sharks whenever they can. Indeed, humans also find salmon sharks palatable and salmon shark charters have become popular in Prince William Sound and Lower Cook Inlet. Fishermen are allowed to keep one salmon shark per day and two per year, and their success rate is high. Sharks caught by commercial fishermen are sometimes also killed, but it's not known how many sharks die in this way each year.

The regime shift is but one explanation for the increased shark populations in Alaska. Sharks may be more abundant due to increases in salmon populations (an important food for sharks), decreases in high-seas gillnetting, or merely a shift to warming waters. Some scientists believe the regime shift and dramatic changes to the ecosystem are the result of global warming flexing its muscles. New evidence for global warming and climate change appears in scientific publications every day; the Arctic Ocean ice cap is much thinner than a few decades ago, carbon dioxide (a greenhouse gas) is at the highest levels in 400,000 years, and continues to increase, and Earth's temperature reached new record highs in the last decade. If global warming continues, you can expect more changes on land and in the ocean, including more regime shifts and changes in the species composition of the Northeast Pacific waters.

Sharks are at the top of the marine food web, so they exert a top-down control that can impact upon the entire food web. Future work on sharks in the Northeast Pacific will look at shark predation effects on such species as salmon, sea otters, and seals. I hope to learn how sharks fit into the Gulf of Alaska ecosystem, and to determine if the changes in their populations are an indicator of more changes on the horizon.

Bruce Wright

Why Plants Make Caffeine

It's Monday again, and somehow I have managed to convince myself over the weekend that waking at 11 is justice, and the natural human way. But here it is, Monday 10:30 am, and I've been up for 5 hours already....

I think it's time for a coffee break.

I rush around, juggling my workload until I can finally manage to fit in 15 minutes for a quick mug-full of that sacred, sacred Joe. But if I were a plant like Cocoa, Kola, Guarana, or Coffee, I wouldn't have had to make the time - I would already have the caffeine built in. Do these plants realize just how lucky they are? That is, of course, assuming that plants use their caffeine to get a buzz on.

In truth, scientists have only begun to guess why some plants produce caffeine. Caffeine is classified as a secondary compound which means it is not essential for the plant's survival. In fact there are many species of caffeinated plants with decaffeinated relatives (poor things), but, as a non-essential component, it can be harder to pinpoint exactly what the caffeine is doing there.

Chemically, caffeine is a methylxanthine. Many methylxanthines are used as pesticides both by humans and plants. It's possible, though not confirmed, that caffeine is used to poison herbivores and plant pests to discourage them from attacking that plant type again; that is, if they survive after metabolising the caffeine. But because caffeine is toxic to plant cells it's stored in specialised cell compartments called vacuoles which are rather like a medicine chest and keep the caffeine safely locked away from the rest of the cell contents until it's needed. Unfortunately this means that the plant doesn't get to enjoy the buzz from its own caffeine (assuming plants can experience a 'buzz'), but that's a necessary trade-off of having a toxic substance lying around.

So it seems that caffeinated plants are lucky to have this compound as part of their natural defences, but it doesn't deter all attackers. For instance, caffeine doesn't poison humans in the doses that we typically ingest (even a Monday morning dose), but it does cause addiction. It works by stopping the enzyme phosphodiesterase from breaking down a signalling substance called cyclic AMP (cAMP for short) and its close relatives. One of the actions of the stress hormone adrenaline is to increase the levels of cAMP in cells, so by preventing cells from breaking down cAMP, caffeine potentiates the action of adrenaline, and gives us a buzz. In even higher doses, and with prolonged use, it can trigger anxiety, muscle tremors, palpitations and fast heart rates, and profound withdrawal effects including headaches, inability to think clearly, and bad moods whenever you mistakenly switch to decaff !

Caffeine-containing plants may be safe from certain insects, vertebrates, bacteria and fungi, but they are preyed on by humans who love the rush it gives them. Not so lucky then, I guess? But there is a hypothesis that plants synthesise psychoactive compounds to target and manipulate humans in particular. In other words, if humans desire the plants, then they will cultivate them. The plants may get processed and eaten up by humans, but because they have been better cared for, they will be able to produce more offspring first. If this hypothesis is true, I think caffeine-producing plants should win whatever the highest international award is for human psychology.

Dalya Rosner

How does DNA Fingerprinting Work?

People everywhere expected the new millennium to bring surprises. But the particular shock and horror that rippled through the international viticulture community in 2000 was most unexpected. It had been found that sixteen of the most highly prized varieties of wine-making grapes were the product of mating between the classic Pinot and the classically undervalued Gouais grape.

This blew the proverbial cork off the industry because the Gouais was considered such an inferior specimen that there were even attempts to ban its cultivation in France during the Middle Ages. This proves that humble origins can still produce superior quality. More practically, though, knowledge of their heritage allows improved breeding of highly desirable subspecies of grape. And viticulturists everywhere had DNA fingerprinting technology to thank.

DNA fingerprinting is a term that has been bandied about in the popular media for about fifteen years, largely due to its power to condemn and save, but what does it involve? In short, it is a technique for determining the likelihood that genetic material came from a particular individual or group. 99% of human DNA is identical between individuals, but the 1% that differs enables scientists to distinguish identity. In the case of the grapes, scientists compared the similarities between different species and were able to piece together parent subspecies that could have contributed to the present prize-winning varieties.

The DNA alphabet is made up of four building blocks – A, C, T and G, called base pairs, which are linked together in long chains to spell out the genetic words, or genes, which tell our cells what to do. The order in which these 4 DNA letters are used determines the meaning (function) of the words, or genes, that they spell.

But not all of our DNA contains useful information; in fact a large amount is said to be “non-coding” or “junk” DNA which is not translated into useful proteins. Changes often crop up within these regions of junk DNA because they make no contribution to the health or survival of the organism. But compare the situation if a change occurs within an essential gene, preventing it from working properly; the organism will be strongly disadvantaged and probably not survive, effectively removing that altered gene from the population.

Left - DNA fingerprints from 6 different people, 1 in each lane (column). DNA can be cut into shorter pieces by enzymes called "restriction endonucleases". The pieces of DNA can then be separated according to their size on a gel. Each piece of DNA forms a band (the white lines on the gel). The smallest pieces travel the furthest and are therefore clostest to the bottom of the gel. The larger pieces travel shorter distances and are closer to the top.

For this reason, random variations crop up in the non-coding (junk) DNA sequences as often as once in every 200 DNA letters. DNA fingerprinting takes advantage of these changes and creates a visible pattern of the differences to assess similarity.

Stretches of DNA can be separated from each other by cutting them up at these points of differences or by amplifying the highly variable pieces. ‘Bands’ of DNA are generated; the number of bands and their sizes give a unique profile of the DNA from whence it derived. The more genetic similarity between a person – or grape – the more similar the banding patterns will be, and the higher the probability that they are identical.

In the non-coding regions of the genome, sequences of DNA are frequently repeated giving rise to so-called VNTRs - variable number tandem repeats. The number of repeats varies between different people and can be used to produce their genetic fingerprint. In the simple example shown above, person A has only 4 repeats whilst person B has 7. When their DNA is cut with the restriction enzyme Eco RI, which cuts the DNA at either end of the repeated sequence (in this example), the DNA fragment produced by B is nearly twice as big as the piece from A, as shown when the DNA is run on a gel (right). The lane marked M contains marker pieces of DNA that help us to determine the sizes. If lots of pieces of DNA are analysed in this way, a 'fingerprint' comprising DNA fragments of different sizes, unique to every individual, emerges.

But why bother? After all, I know where my wine comes from – Tesco's, right? Well, there are many relevant applications of DNA fingerprinting technology in the modern world, and these fall into three main categories: To find out where we came from, discover what we are doing at the present, and to predict where we are going.

In terms of where we came from, DNA fingerprinting is commonly used to probe our heredity. Since people inherit the arrangement of their base pairs from their parents, comparing the banding patterns of a child and the alleged parent generates a probability of relatedness; if the two patterns are similar enough (taking into account that only half the DNA is inherited from each parent), then they are probably family. However, DNA fingerprinting cannot discriminate between identical twins since their banding patterns are the same. In paternity suits involving identical twins - and yes, there have been such cases - if neither brother has an alibi to prove that he could not have impregnated the mother, the courts have been known to force them to split child care costs. Thankfully there are other, less “Jerry Springer-esque”, applications that teach us about our origins. When used alongside more traditional sociological methodologies, DNA fingerprinting can be used to analyse patterns of migration and claims of ethnicity.

DNA Fingerprinting can also tell us about present-day situations. Perhaps best known is the use of DNA fingerprinting in forensic medicine. DNA samples gathered at a crime scene can be compared with the DNA of a suspect to show whether or not he or she was present. Databases of DNA fingerprints are only available from known offenders, so it isn't yet possible to fingerprint the DNA from a crime scene and then pull out names of probable matches from the general public. But, in the future, this may happen if DNA fingerprints replace more traditional and forgeable forms of identification. In a real case, trading standards agents found that 25% of caviar is bulked up with roe from different categories, the high class equivalent of cheating the consumer by not filling the metaphorical pint glass all the way up to the top. DNA fingerprinting confirmed that the ‘suspect’ (inferior) caviar was present at the crime scene.

In the example shown on the left, DNA collected at the scene of a crime is compared with DNA samples collected from 4 possible suspects. The DNA has been cut up into smaller pieces which are separated on a gel. The fragments from suspect 3 match those left at the scene of the crime, betraying the gulty party.

Finally, genetic fingerprinting can help us to predict our future health. DNA fingerprinting is often used to track down the genetic basis of inherited diseases. If a particular pattern turns up time and time again in different patients, scientists can narrow down which gene(s), or at least which stretch(es) of DNA, might be involved. Since knowing the genes involved in disease susceptibility gives clues about the underlying physiology of the disorder, genetic fingerprinting aids in developing therapies. Pre-natally, it can also be used to screen parents and foetuses for the presence of inherited abnormalities, such as Huntington’s disease or muscular dystrophy, so appropriate advice can be given and precautions taken as needed.

Dalya Rosner

Big Fish, Little Sea

Alongside their neighbours on coral reefs, few fish come close. They can even outsize turtles and sharks. With sad-looking lips and inquisitive eyes their faces are decorated with intricate blue-green scribbles resembling New Zealand Maori war paint, hence their other name is Maori wrasse. Napoleon wrasses are found on reefs across the Indian and Pacific Oceans and for my PhD I study them both on a pristine, remote atoll in the South China Sea and around the coral fringed coast of the northern Borneo.

Sadly it is becoming increasingly rare to catch a glimpse of the majestic Napoleon wrasse in the wild. You are more likely to see them swimming around tanks in expensive seafood restaurants in Hong Kong or Singapore. Since the 1970's it has become a prestigious delicacy to dine on large, colourful coral reef fish that are killed moments before cooking. The Napoleon wrasse is an especially favoured status symbol. A plate of their rubbery lips sells for 250 US dollars and a magnificent 40 kilogram specimen can cost as much as 10,000 US dollars.

Despite the high value of these fish, and the growing demand, very little is known about Napoleon wrasses, their biology, how they are exploited, and how remaining populations might be protected from extinction. But what is clear is that this big fish is in big trouble.

Various features of the Napoleon wrasse biology make them especially vulnerable to overexploitation. Like many other large animals they grow slowly and take years to reach maturity, which means populations take a long time to recover from even low levels of hunting.

Their mating system also predisposes Napoleon wrasses to being heavily fished. During each new moon they congregate to mate at specific locations on the reef. Like lions in the African savannah, each group of Napoleon wrasses has a dominant male who does most of the mating. He stakes out his territory, fiercely chases off intruding males and mates with the dozens of females that arrive. The timing of these spawning aggregations is highly predictable. In the population I study the females begin to arrive at 12.30pm, and everything is over by 3pm. The problem is that if fishermen learn the precise timing and location of these aggregations, then they too can lie in wait and catch many more fish than they would at other times by painstakingly hunting for these otherwise solitary fish.

The live reef fish market demands two distinct sizes of fish, both smaller "plate sized" individuals enough for a single diner, as well as outsized adults that will impress guests at a banquet. Either way this spells bad news for the wild populations of Napoleon wrasses. The smaller fish are juveniles, taken from the wild before they have had a chance to reproduce. As for the large fish, these are all males and their removal potentially leads to a serious female bias. This is because Napoleon wrasses start off life as females and undergo a sex change when they grow to a large enough size, but this takes time.

It seems that Napoleon wrasses just aren't cut out for high levels of exploitation and my data are backing this up. I have collected thousands of records of Napoleon wrasse sales from fisheries in northern Borneo going back for nearly ten years. Graphs show that the number and size of Napoleon wrasses caught by each fisherman has taken an unmistakeable and disheartening nosedive over the years. This suggests that there are few Napoleon wrasses left and fishermen are struggling to find them.

The sales records also show another very worrying trend. As the Napoleon wrasse become a rarity their status and exclusivity escalate so that diners are prepared to pay even more inflated prices. As prices are driven higher, so is the incentive for fishermen to catch the last remaining fish.

What can be done to help? As with most fisheries, there is no easy answer. Just like the blue fin tuna or North Sea cod, there is too much demand for too few fish. If the trade were to be banned, fishermen would lose their jobs, but when the fish have gone there will be no trade and no jobs.

There is however a glimmer of hope for the Napoleon wrasse. Not all countries that could trade in live Napoleon wrasses actually do so. The trade is banned in the Seychelles and the Maldives and licences are strictly regulated in Fiji. These and other countries are beginning to realise that by leaving Napoleon wrasses on the reefs they can gain from scuba diving dollars.

The question is who is prepared to pay most in the long run, diners or divers?

Helen Scales

Transposons: Spam from the Dark Ages

Pretty much everyone who has ever had an e-mail address will have come across "spam", that trickle (or flood) of unsolicited junk e-mail offering to sell you anything from viagra to a share in a dead dictator's fortune. Most of us just delete them with a touch of irritation at their clogging up of our mailboxes, and promptly get on with whatever we were doing.

But looking inside ourselves, we discover that this phenomenon pre-dates the internet, and even cave drawings and flint axes. Each cell in our bodies contains thousands of copies of "biological junk mail", except this kind is made of DNA instead of words and data packets. Indeed, while only 2% of our genome directly codes for the proteins that make up our bodies, over 40% of the remaining 'non-coding' DNA is filled with spam! What are these biological "junk mails"?

They are called transposable elements, or transposons, and are ubiquitous throughout life. They were first discovered by Barbara McClintock in 1944 when, noticing some unusual and changing colour patterns in the kernels of some maize she was studying, she hypothesised the existence of mobile genetic elements to explain the phenomenon (see figure 2, below). With the explosion of molecular biology, much more is now known about these jumping pieces of DNA.

There are two broad classes of transposable elements. DNA-based transposons, which are responsible for the colour changes in maize, move around the genome in a "cut-and-paste" fashion, literally cutting themselves out of their original location and inserting somewhere else. RNA transposons, or retrotransposons as they are also known, work differently. They are thought to originate from viruses that have inserted (integrated) themselves into the genome of a cell they have infected, where they lie dormant and are passively copied along with the host cell's DNA every time the cell divides. Over time, these "sleeping" viruses can mutate, just like any other part of the host's genome, and these mutations can lead to them losing their ability form new virus particles and infect new cells. However, they often retain, at least for a while, the ability to copy themselves, and these copies can, in turn, be inserted somewhere else in the host genome. So while DNA transposons "jump", retrotransposons "copy" themselves to new locations. This is illustrated in figure 3, below.

Figure 2 : Colour variations in maize caused by DNA transposons. A normal gene (Bz) gives maize kernels a dark colour (left), whereas a mutant version (bz) confers an orange colour (middle). If the gene is disrupted by a transposon (bz-m) this also results in an orange colour, but in some of the cells in the kernel the transposon has jumped back out of the gene, restoring its function, producing dark spots where this has happened (right).

So what is the point of all these jumping bits of DNA? Can we simply ignore them as a biological oddity, or is it important to understand them? Well, just like the spam we receive by e-mail or post, most of them sit harmlessly in a corner of our genome, but some copy themselves and jump to new locations in our DNA where they affect adjacent genes. In their new location they can disrupt a gene completely, or subtly change the way it exerts its effects in the cell. This can have both positive and negative consequences.

Transposons have undoubtedly been a source of genetic diversity throughout evolutionary time, providing raw material on which natural selection can work. For example, every one of our genes is under the control of another stretch of DNA sequence called a promoter which influences when the gene is turned on and off, and what at level it is expressed. Parts of transposons are known to behave like promoter sequencess and when they jump next to a gene these extra promoter segments can change the way the gene is regulated. If this change happens to be beneficial, it will be selected for in evolution. Indeed this seems to have happened frequently, and it is estimated that 25% of human promoters contain sequences originally from transposons.

In rare cases, single transposons may have had a profound effect on human evolution. The most common transposon in humans is called Alu. Alu elements are DNA transposons found only in primates and seem to have been most active between 30 and 50 million years ago. Researchers have noticed that Alu contains sequence which looks very similar to other parts of the human genome that are regulated by hormone-binding proteins. These are proteins which allow hormones to interface with our DNA, regulating whole sets of genes at once. If Alu's also have this property, then they may have caused widespread changes in the way genes respond to hormones when they jumped near active genes.

Our immune system may also owe a lot to the action of a particular transposon. Our ability to make antibodies to any microbe that infects us relies on a particular set of genes in the B cells of our immune system that can be shuffled around in near-limitless combinations. This means that with a relatively small set of "base" genes, our B cells can produce antibodies on demand against whatever infection we might be facing, without needing one gene for every possible antibody. However, this requires proteins that can "cut-and-paste" DNA to create these new combinations. We've seen this phrase before already … this is how DNA transposons move around! Scientists have found that the proteins that make our antibody-shuffling system possible, called RAG proteins, entered the genome of our ancestors on a DNA transposon around 450 million years ago. This allowed the jawed vertebrates to adapt their immune responses to each case of disease, a major improvement on the more limited innate immune systems present before.

Figure 3: DNA and RNA transposons move around the genome. DNA transposons cut themselves out from their original location, and insert themselves somewhere else in the genome. RNA transposons make a copy of themselves that inserts into a new location, leaving the original transposon intact.

Negative consequences of a transposon jumping into a gene are more likely though. Transposon insertion into a gene can scramble the coding sequence, producing a defective or truncated gene product with little or no function. It can also be detrimental in other ways. Even if it doesn't insert into the coding part of the gene, it can still cause problems, such as altering its regulation in dangerous ways by disrupting the promoter sequence.

Figure 4: Xenotransplantation - pigs are a potential source of organs. But when scientists transplanted pig organs into mice, they found that a porcine (pig) endogenous retrovirus, which had been dormant in the pig genome, reactivated and infected the mice.

With more and more genomes being sequenced, transposons can help reconstruct the tree of life. By looking at the pattern of transposons present in different organisms, and how they have mutated over time, inter-relationships between species can be inferred. For example, three ancient retroviral insertions are present in exactly the same places in the genomes of deer, giraffes, hippos and whales. This is just one piece of evidence linking whales to their land-dwelling ancestors.

Transposable elements can also be both a blessing and a curse when it comes to manipulating technology for our own benefit. On the plus side, they are seen as one of a number of possible vectors, or delivery systems, for use in gene therapy. If an efficient way could be developed to smuggle engineered transposons into live human cells in the body, they could be used to deliver healthy copies of a gene that is defective in a patient suffering from a genetic illness.

One area where they can present an obstacle is xenotransplantation, the use of animal organs for human transplants. Pigs in particular are seen as a promising source of donor organs. However, when scientists transplanted pig organs into mice, they found that a pig endogenous retrovirus, or PERV, which had been "sleeping" in its host, became active and infected the mice (it had not yet entirely lost its ability to jump to new cells). Though the mice didn't seem to suffer any symptoms, it would be considered too risky to try on humans without a better understanding of the consequences.

So it seems that transposons have gone hand in hand with life ever since there has been DNA to hitchhike on, and there is certainly no delete button for this particular brand of spam. For better or worse, it's here to stay. Now if we could just do something about all these junk mails...

Jamil Bacha

What is the purpose of sexual reproduction ?

SEX: A short word. Often used. Often used to sell products in fact. Yet it is one of our base instincts, one of our prime motivations in life. I can't remember how many times I chose a seat on the train because a good-looking girl sat nearby, or bought a magazine because of the attractive woman on the cover. So why do we find the opposite sex so attractive?

I mean, the act of sex itself is a pretty bizarre thing to do, all that jigging around and what about the mess? I mean we all look pretty hilarious whilst we do it (and the only reason they don't look daft in films is because they are not really doing it). If we didn't enjoy it so much would we really bother?

Would you go through all that if it weren't for the orgasm at the end? After all, there is a lot more to it than just the act of sex itself. There is the whole elaborate (and expensive) courtship display beforehand: the "asking her out", the "first date", a bit of food, a bit of wine, one thing leads to another... (Not on the first date, of course). Then there's the "I'd like to do this again sometime" and the 'should I call today, or wait a few days? I don't want to seem too keen'. Countered by "I'm washing my hair tonight". And so back to square one, until you get past the 'hair wash barrier'. Now you're in with a chance!

So basically we are all driven with a deep desire to mate and we will go through just about anything to achieve it (girls, the best time to ask a guy for that expensive treat is just beforehand). I remember all the embarrassing episodes that happened when I was a teenager. Many left me scarred for life, but none stopped my adolescent craving to 'go all the way'.

Propagation of Species.
So a lot of questions, Adel, but what point are you trying to make? Well, I'm trying to make the point that sex is meant to be all about propagation of species or more specifically, it is all about propagation of our genetic material. But is the theory that we are simply vessels for the propagation of genetic material a little simplistic? As I alluded to above, there is a lot more to finding a mate than simply sex. If passing on genetic material is what it is all about why don't we just clone ourselves? No mess, no fuss, just pure transmission of your own genetic material! Many primitive animals do it every day. Some do it several times a day!

Which begs the question is there an advantage to sex? The whole point of sex is to mix the genes in the gene pool allowing the transmission of 50% your own and 50% your partner's genes to your young. The point of mixing the genes is to allow for variation in the gene pool. As genes are mixed new combinations arise some are useful to the survival of a species, others are detrimental. Those that carry detrimental genes are disadvantaged at mating and are thus less likely to pass on those detrimental genes. In contrast, those that possess genes, which confer an advantage, are more likely to survive predators and beat their competitors in the race to find a mate, and their genes are more likely to be passed on. This is the basis of Darwin's theory of evolution and the mechanism by which it happens is termed Natural Selection.

Monogamy versus Polygamy
So if the whole point of sex is to mix up the gene pool why not have multiple partners rather than a monogamous relationship? Why are humans (generally) monogamous, are we the only creatures to spend the majority of our lives with one partner? Is that what puts us apart from other animals? Not so. Take love birds for example, they remain in lifelong monogamous pairs, but they seem the exception rather than the rule. In contrast, many animals belong to the 'sowing wild oats' school of thought, for example, the male chimpanzee often invites females to mate by typically spreading his legs to reveal a bright red, erect penis that stands out against the black scrotum. Not recommended behaviour down the pub on a Friday. Similarly, some human males are of the 'kebab theory of women': a great idea after ten pints down the pub, but you wouldn't want to wake up next to one every day. More seriously, creatures such as fish and especially sea urchins release their eggs and sperm into the sea and hope that some of each meet up and fertilise. Not strictly polygamy, granted. But if humans mated with numerous partners their genes would be spread further and as such, is monogamy not a disadvantage? The answer here may be quality not quantity. Monogamy in humans may have evolved because we need to nurse our young for many years before they become independent. A stable family life is important in order to make our offspring high achievers and thus attractive to other high achievers. In other words, by improving the quality of young we increase the chances of propagating our own genes successfully.

What's Love got to do with it?
OK. I've established we need sex and that for humans monogamy is preferred. So where does love fit into all this? Pah! I hear you say. "Love? That's not very scientific, is it? This essay is about the science behind sex, not the spiritual and mysterious nature of love.

"Aha!" I reply. But has love evolved to maintain monogamy? Those possessed by love will do many (often strange) things and unless you experience it yourself, one cannot explain how it can be an incredibly strong motivator. Arguably stronger than lust, and that's saying something! Many people have married 'the One', citing that they just knew it in their heart 'that was it'. Love is strong enough to keep couples together through thick and thin. 'All you need is love'. I wonder if there is some physiological basis to love? Perhaps it could be a balance of hormones that subtly affect our mental perceptions of our chosen partner versus other acquaintances. A little like the release of endorphins during pleasurable activity. But I suspect it is a higher cerebral function modified by social conditioning and cultural values. I'm no neuroscientist so I won't explore avenues I know little about.

What I want to argue is that the whole point of falling in love is a complex form of mate selection. A bit like the female peacock (peahen) that picks the peacock with the biggest and best-kept tail. As I hinted at before, it is women that are the choosy ones; the men are less so (driven by a deep desire to distribute their genes far and wide). So men need to attract women, and women need to choose a good husband and father. It is not something taken lightly and so love has evolved as a mechanism to secure a good mate and keep them together, at least until the kids have flown the nest.

The Evolutionary Arms Race
But why should we evolve? What's the point? Is there some spiritual force behind it all pushing species to evolve to perfection? Possibly, but it is not for the scientific method to explain matters in that way, that is for the philosophers to argue. One interesting theory raised in the book 'The Red Queen' is that sex has evolved as a protection against parasites. Daft, eh? Well, no. Let's break it down a little. Sex evolved to allow genetic variation. Genetic variation allows evolution to select the most hardy. Why do we need to be the most hardy. The answer is to beat infections, especially 'genetic infections': the viruses. A virus is a small collection of genes that hijacks cells to take over their machinery to reproduce. Cells evolved mechanisms to keep viruses out, the viruses struck back by evolving ways around these defences. Cells retaliate by creating new and better defences. So the arms race continues. Such models have been run through computers comparing sexual versus asexual species and how they cope with a parasite invader. In all cases, asexual populations were wiped out within a few generations whilst sexual populations survived.

Of course there are other theories, such as sex was useful millions of years ago to ensure survival and was something we've been stuck with since, a sort of evolutionary left over. But the parasite theory is one that has a very convincing basis.

Outstanding questions to think about...
Why do we only have two sexes? Why not three or more?
Why is our sex ratio 1:1?
Why are we not hermaphrodites (both male and female at the same time)?

Adel Fattah