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