What's So Great About Sex?

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What's So Great About Sex?

One of the great puzzles in biology is the origin of sexuality. Not all organisms reproduce sexually, but pretty much all of the big animals do. Many creationists, skeptical of any evolutionary explanation for the emergence of sex, argue that sex is an irreducibly complex mechanism. They say that there is no way to get from asexual reproduction to sexual reproduction, since it would take two organisms, each evolving randomly and separately into compatible sexual partners. The odds against this are so staggeringly bad, they say, that we can know for certain that sex did not evolve.

I do not intend to refute all of the creationist arguments here, nor do I intend to propose a complete theory of sexual reproduction. Frankly, if creationist arguments seem convincing to you, it would be best for you not to waste your time. Stop reading now. There's a certain level of credulity with which I cannot compete. For those of you still with me, what I intend to do is give you an introductory understanding of many of the biological mechanisms involved with sexual reproduction. Once we have a basic understanding of what sex does for us biologically, we can begin to build up to understanding what it does for us as complex cultural organisms. I promise that we'll get around to talking about dating and making out and getting laid, but not until we're better prepared.

If you're especially interested in the current theories about the cause of sex, see the list of recommended reading at the end of this chapter. In order to keep things on a layman's level, I'm going to avoid the topic. It's rather esoteric, and is not especially pertinent to my end goal, which is examining human nature and human sexuality as objectively as possible.


Asexual vs. Sexual

At first glance, sexual reproduction seems to be a bad idea. Many organisms can simply split themselves in two. This leads to exponential growth, which is good for an organism. In sexual reproduction, it requires two individuals to make offspring. In other words, half as many reproductions are taking place. All things being equal, asexual organisms should out-breed, and therefore, out-survive sexual organisms. The history of evolutionary science is riddled with new discoveries that seem to indicate that sex is a luxury, not a necessity.

Before we go on, we need to understand a few terms. I promise we won't get too bogged down in scientific jargon, but in this case, learning a few words will save you from having to read long descriptions over and over. First, meiosis is the word for the selection of genes that will go into a sex cell. In any sexually reproducing organism, each parent's genes are only partially passed on to the offspring. During meiosis in humans, each of the 23 pairs of chromosomes is laid beside its opposite, and then chunks of one side are swapped with chunks from the other side. (The number of pairs of chromosomes varies widely in different species.) This is called recombination. Once the new set is finished, it is passed on to the offspring, and will be combined with a set from the other parent. This is called outcrossing.

Sex, essentially, is recombination plus outcrossing. This is different than the reproduction of bacteria, who, like ships in the night, pass each other and swap genes, then go their separate ways, to divide at some later time. In sex, we get a thorough mixing of genes from each of our four grandparents and our two parents.

Sex confers many benefits. Perhaps most notably, it repairs genes. DNA, you might know, is made of four chemical bases, which we designate A,C,G, and T. Each letter is complimentary to another. T and A are natural pairs (make your own joke here. It's ok.), and C pairs with G. Because of this, there's a really simple way to repair DNA. As you might also know, DNA's famous double helix shape is basically two strands, each a complementary copy of the other. If one section consists of TTCAAG, it's complementary section will be AAGTTC.

Where this comes in handy is when one of the sections becomes damaged. Light, cosmic radiation, and other factors are constantly damaging living cells and the DNA contained within them. Special enzymes move up and down the strands, looking for damage. When they find a damaged section, they simply reference the other side of the DNA strand to figure out which of the four letters needs to be inserted in the damaged area.

There is something in nature that at first glance seems a better alternative to this complicated process. Just as a hard drive keeps backup copies of important files, organisms could keep 'extra' copies of their DNA. That way, if a particular segment was damaged, there would still be viable copies. As it turns out, this does happen quite a bit in nature. It is called diploidy. Most plants, and nearly all animals are diploid, meaning that they have two copies of each gene, one from each parent. Some animals and many plants are polyploid, having three or more copies. In diploid animals, only the sex cells, the egg and sperm are haploid, meaning that they have just one copy.

If diploid organisms performed recombination during normal cell division, there would be plenty of cell repair, but they don't. Recombination only happens during meiosis, which means that sex is the opportunity for a species to refresh the integrity of its DNA. If you think about it, this is very economical. During normal cell division, cells with damage will ordinarily die out, and the undamaged ones will generally survive. Sex, on the other hand, is a one shot deal, and it's really important to get it right.

(As a side note, you should realize that I'm taking a great deal of liberty in describing these chemical reactions as intelligently motivated. This is for ease of understanding, and does not indicate that there actually is any intelligent direction. These processes work because that's the way chemistry works. The molecules are blind and dumb, in the same way that vinegar and baking soda, when mixed, are not consciously producing a violent chemical reaction – yet a reaction is produced.)

All of this repair work is conducted more or less constantly while an organism is alive, so where does sex come into the picture? Imagine now that both strands of DNA are damaged. The enzymes have no point of reference, and cannot 'know' which letter needs to go where. This is where the two processes involved in sex come into the picture. Through recombination and outcrossing, a new template is introduced, and the new organism will not inherit the damaged DNA. As you can imagine, this is of great benefit to the offspring. Sex, then, is a way of repairing DNA across generations. Though the parent may be flawed, the offspring will not be.

There are other kinds of changes in DNA besides damage. Mutation is essentially an error in copying. Most mammals accumulate mutations at a rate of approximately one hundred per genome per generation. Of those one hundred, ninety-nine will most likely not matter, for much of our DNA is superfluous, and many mutations are neutral, contributing neither good nor bad effect to the organism. How does sex affect mutations? Simply put, it is highly effective at distributing good mutations throughout the population.

In any technological industry, espionage and theft are par for the course. It's simply too much to ask a Research and Development Department to develop something from scratch when there's a perfectly good working model across the street at a competing business. In the same way that the television or automobile industry borrows (steals) from its competitors, so do individuals within sexually reproducing populations. If an individual develops a beneficial trait through mutation and then sexually reproduces, each of its offspring are potential carriers of the mutation. Within a few generations, each of the mutated offspring have sexually reproduced, and now there is a widely varied population.

By contrast, bad mutations tend to die out because they are less likely to reproduce successfully. The benefit of sexual reproduction is still evident, for recombination and outcrossing will still tend to eliminate mutations, in the same way they eliminate damaged DNA. The beauty of sexual reproduction is that the offspring who do inherit good mutations will tend to reproduce more effectively. Though all children of parents with good mutations will not share the mutation, those that do will reproduce more successfully.

These processes are very slow. In fact, there's a real problem with them. Even accounting for the positive benefits of sex, there is an accumulation of bad mutations. Consider a group of ten water fleas. One of the fleas has no mutations in its genes, and the rest have one or more. Now suppose that five of the fleas will be eaten by fish before they reproduce. The mutation free flea has a one in two chance of reproducing. The one with five defects has the same chance, but there's a catch. If the mutation-free flea does not reproduce, the only way to get back to mutation-free in the population is for one of the existing mutations to mutate back to not being mutated. This is, of course, extraordinarily unlikely. This means that successive mutations accumulate. Since the majority of mutations are either neutral or bad, this spells trouble for sexual reproduction. This phenomenon is called “Muller's Ratchet.” (Think of a ratchet from your tool box. It does work when you turn it one way, but you can't go the other way with it and do anything productive. Your only choice is to continue turning the nut in the direction it was already heading.)

I promised that we won't be getting into heavy duty biology, and I will stay true to my word. Suffice it to say that there are several rather complicated genetic theories as to why sexual reproduction continues to work successfully in spite of the ratchet, but all of them have problems. Each of them represents a partial solution to the problem, but none of them, singly or in conjunction, completely explains why sex is still so successful. Everything we've talked about so far is genetic, and the fact is, ecology has a lot to do with sex, too. It is very likely that no single explanation from a single scientific discipline will be completely successful at explaining the success of sexual reproduction.

Before we go on, I want to make sure you understand a very common logical fallacy – the affirmation of the consequent. If we were to visit my house one afternoon, and upon arriving, we noticed that the yard was wet, we could speculate as to the cause of it being wet. You could suggest that it might have rained recently. Rain certainly can cause yards to become wet. I might point out that I have a sprinkler system in my yard. Sprinklers also can wet yards. For that matter, my neighbor has a hose long enough to reach my yard. He might have watered my yard with his hose.

The fact is, any of these are possible explanations, and each would be scientifically acceptable. However, we cannot know for certain that any one of these was the cause of my yard becoming wet. There are yet other possibilities, and there is the very real chance that more than one of these events happened in succession. If I say, “My yard is wet, and rain wets yards. Therefore, rain wet my yard,” I am affirming the consequent, and making an error in logic. (I might be correct, but it would be because of luck, not good logic!)

Returning to sex, we must remember that while sex does confer a lot of benefits, it is a mistake to say that sex happened because of these benefits, or that any one of them is the cause of it all. Not only is it affirming the consequent, but it's breaking a fundamental law of evolution. Natural selection is not forward thinking. It responds only to current conditions, and cannot predict that something will be beneficial in a thousand generations. Genetic repair is great, but it would not have benefited the first pair of sexually reproducing organisms. Clearly, there is something else involved.


More About Fleas

At the time of this writing, there are so many misconceptions about evolution in the average American's mind that it's hard to recognize it as the same concept that scientists study. Some of them are a result of mis-characterization by creationists who want to teach Intelligent Design in schools. Others are the result of simple misunderstandings. Like other myths, the misconceptions about evolution become so entrenched in our culture that it's almost too much to expect that anyone would bother to examine their own beliefs.

When most people think of evolution, they think of something that is working towards a goal. It seems that humans especially are getting bigger, faster, stronger, and smarter. Evolution itself must be progressing towards some pinnacle of life, some perfect form of existence. Perhaps we can be forgiven for making this assumption. After all, just about everything humans do is designed to make something better. We are goal oriented beings, and part of what makes us human is our tendency to see humanity in other things. This is known as anthropomorphic bias, and it is part of what helped us survive our early days in the savannah. Unfortunately, it also causes problems when we see human-like traits that are not actually there.

In any case, evolution is actually not goal oriented, and in fact, if it were to have a goal, it would most likely be stasis. If you think about this for a second, you will see the truth in it. Sharks, roaches, and other extremely well adapted organisms haven't changed much in millions of years. It's the old adage: “If it ain't broke, don't fix it.” For a top predator in a stable environment, virtually any change will be detrimental. If something is adapting quickly, it is because something is forcing it to do so. This leads us to our next misconception about evolution.

Many people think that evolution is life versus the environment. We imagine meteors and earthquakes and climate changes as being the driving forces behind evolution. In fact, the environment is usually remarkably stable, and doesn't contribute very much to natural selection. In World War I, 25 million people were killed in four years. In World War II, not two generations later, 72 million people died – almost 4 percent of the population. By contrast, the Sumatra-Andaman earthquake, which caused the tsunami of 2004, was responsible for only 275,000 deaths.

Intraspecies and interspecies competition, that is, competition within a single species and between species, is responsible for far more evolutionary impetus than the environment. The numbers I have just given are not meant to prove this point, only to show that our perception of evolution is skewed. If you think about the animal kingdom for a second, though, you will realize the truth of this idea. Many animals have hundreds, or even thousands of young, each of which is competing against its own kind for resources, and trying not to get eaten by predators. Many animals have multiple offspring, and then either kill all but one, or let them fight it out for themselves, until only the strongest remains.

There's an apocryphal tale of two scientists in the woods. They encounter a large bear and begin running away. One looks at the other and says, “There's no way we can outrun a bear! We're doomed!” The second replies, “I don't have to outrun the bear, friend. I only have to outrun you.” This story illustrates the balance of competition. Not only are organisms trying to avoid predators, they are trying to outdo their own kind, both for survival and resources. This is a very good analogy for evolution.

There is yet another part of the picture, though. Competition is not just limited to peers and predators. There is another type of creature that has caused more evolutionary adaptation than any other, and not just by a little bit. You might never think of it, but I will give you another number to compare to those I gave you for the World Wars. After the first World War, there was an influenza epidemic that killed 25 million people – the same number as the entire war. The flu, however, only took four months to do its dirty work. It was only one out of thousands of parasites that took human lives. Humans are only one of millions of life forms.

The black plague, smallpox, measles, syphilis, and tuberculosis are just a small representation of the thousands of parasitic organisms that have killed humans over the millenia. Not only have parasites killed humans, but every other “higher life form” on the planet. Parasites are short lived, reproduce extremely fast, and spread very effectively. By the time you die, the bacteria in your stomach will have passed through more generations than all of the generations of man that have ever existed.

There is an evolutionary arms race in which parasites and hosts battle for stasis. If the parasite kills off all of its hosts, it will die. If the host develops immunity, the parasite will die. A balance must be achieved if both host and parasite are to survive. Actually, the term “arms race” is not adequate. In a human arms race, old weapons become obsolete, and are never useful again. In evolution, it is not so. If a host develops an immunity to a certain parasite, the parasite itself will adapt. Soon, both the host and the parasite will not “remember” the genetic reasons for their previous success. Over the generations, the old, obsolete methods of parasitism will be selected out of the gene pool, for they are no longer useful. This leads to the very real possibility that in future generations, a parasite may go backwards and “rediscover” an old means of attack that the host has “forgotten.” Thus, evolution is not necessarily an ever-increasing race between foes. Instead, it is more like running on a treadmill. If you don't keep up, you will fall, but you aren't really going anywhere specifically.

Keep in mind that a flea needs a dog. Parasites evolve very quickly due to their very short generations. Larger animals need to be able to adapt very quickly if they are to survive the overwhelming numerical power and genetic adaptability of their tiny adversaries. Sex conveys effective methods for distributing mutations rapidly through populations – advantages that asexual reproduction simply doesn't have access to. Fleas themselves have tiny parasites to which they must constantly adapt. If anything, the only constant among “higher animals” is that they have parasites which are doing as well or better at surviving.

To get a little more specific, the arms race, or more properly, the treadmill race, is all about proteins. Viruses, bacteria, and fungi all try to get into host cells with what amounts to a biological key – a protein molecule that essentially binds with the host cell, allowing the genetic contents of the parasite to invade the host cell. This is where sexual reproduction begins to gain such an advantage. An asexual species will have all the same locks. If a parasitic organism gets the key, it's quite easy to wipe out the entire group. Sexual reproduction, on the other hand, disperses many different kinds of locks, even within very close relatives. The benefit of this kind of diversity is obvious.

In essence, sexual creatures have a library of locks from which to choose when reproducing. This is called polymorphism. The benefit of polymorphism can be seen clearly by looking at sexually reproducing creatures that have had the library reduced through inbreeding. Wheat, for instance, has been selectively bred through many generations of successive inbreeding, for the purpose of creating consistent (and better) yield for farmers. The end result, though, is that this inbreeding opens the door for epidemics that can only be cured with more and more pesticides, which, as we all know, simply creates more resistant strains of parasites. The cycle does not improve until more diversity (and more chance for changing locks) is reintroduced into the equation.

Again, I must caution the reader about jumping to conclusions about what caused sex. At present, we simply don't know what the exact sequence of events was. It might have been a combination of factors, and it might have been something that we haven't discovered yet. This is one of the reasons that science is such a dynamic field. No matter how many questions you answer, there are still more to be considered. At this point, though, we know quite a lot about sex. It conveys many evolutionary advantages: genetic repair, spreading good mutations, minimizing bad mutations, and creating rich diversity. (Consider that the humble mushroom hasn't changed much in centuries because it's pretty much impossible to genetically engineer asexually reproducing organisms. In contrast, we have thousands of varieties of sexually reproducing food plants that we have genetically engineered.) Finally, it is only by a combination of these and other benefits that we could hope to genetically outwit the multitudes of parasites that are not going anywhere anytime soon. In short, the exact evolutionary history of sex may still be somewhat mysterious to us, but the reasons for its continued success are clear.


Gender Wars

Now we know all about the advantages of sex, and we've been introduced to a remarkable concept of evolutionary theory, namely the treadmill. An even better analogy can be drawn from Alice in Wonderland. At one point, Alice finds herself running alongside the Red Queen, a chess piece that continually ran, but never got anywhere because the landscape kept up with her. The Red Queen (also the title of a brilliant book by Matt Ridley on the subject of sex and evolution) is a brilliant analogy for the kind of path evolution takes. Instead of climbing ever upward towards some perfect state of rest, all life is in a constant struggle against itself, its predators, and its parasites. Each advance by one of the three results in an advance in one of the others. There is sometimes a brief period of rest when an organism has developed a distinct advantage, but it will not be long before the tables have turned and everything else has adapted, making it once again obsolete. As we have seen, the progression need not be linear. It is simply a matter of finding what works.

Even more astonishing is that this system is not just at work between multicellular organisms. It also exists in genes themselves. In his remarkable book, The Selfish Gene, Richard Dawkins explained how some genes exhibit behaviors which are detrimental to the organism they helped to 'build.' This can also be seen working between parasites and hosts, as in dogs with rabies who bite as many other dogs as possible, only to the benefit of the virus, not the dog.

Gender itself appears to be the result of this kind of chromosome competition. During meiosis, the formerly diploid cells become haploid sperm and egg. This is the one chance for selfish genes to assert themselves. Think of it this way: When a woman conceives, her baby gets only half of her genes. These are the survivors which will live on for at least another generation, and may well be passed on to hundreds or even thousands of offspring in just a few more generations. The others are relegated to extinction, except on the amazingly rare chance that exactly the same genes will make it into another egg in the future, and get a second chance.

Suppose that a gene figured out how to kill the gene with the same number on the opposite chromosome? That gene would ensure survival for itself, at the expense of the other. In fact, such genes do exist, but they are quite rare. At the risk of oversimplifying to the point of absurdity, the basic idea is that “killer chromosomes” are dependent on a chemical to do their dirty work. Since they are the same as their neighbor, they must have a chemical repellent, of sorts. This is all fine, except that chromosomes sometimes swap. That is, in most animals and plants, it is common for chromosomes to switch sides. This is called “crossing over.” It is just fine for most chromosomes, but for “killer chromosomes,” it is suicide, for they leave their protective repellent behind, and are exposed to the very weapon they would have wielded against their neighbor.

Now that we understand the principle of the selfish gene (if only generally), we can look more closely at the sperm and the egg. When a sperm fertilizes an egg, only the nucleus gets into the egg. Some genes are left behind in organelles, which use oxygen to make energy from food. These organelles are descendants of bacteria that were part of the eucaryotic revolution. That is, complex cells formed as prokaryotes essentially absorbed each other, becoming symbiotic. We should not be surprised that in the same way that the ancient bacteria “learned” how to exploit others, these organelles learned to behave in ways that were beneficial to themselves.

When we ask the question, “Why are there two genders?” we are asking why these organelles are inherited only through the mother. It seems a lot of trouble to create complicated systems to keep one set of organelles out of the egg, but that's exactly what has happened. The answer is a war of attrition. If organelles of both male and female parents were allowed into the egg, the competition would leave both sides depleted, and the entire organism weaker for the exchange. There is, in fact, an organism that does just this. It is an alga called Chlamydomonas, and instead of male and female, it has plus and minus. The two sets of chloroplasts fight it out until only 5% of the original material remains. The whole cell suffers as a result.

In humans, we have a rather advanced way of handling the problem of gender wars. Instead of arranging for one set of chromosomes to be destroyed, we simply leave them out of the egg to die. In doing so, it is theorized that we avoid many potential infectious organisms that might be tagging along inside the organelles. In other words, our gender is the result of a peaceful resolution to a competitive problem. In a very real way, the war of the sexes begins on a cellular level!


Gender Wars II: Class Wars

When we examined cultural myths and their effect on our perceptions of sexuality, it became obvious that we have an unfounded tendency to view ourselves as separate from the other organisms on earth. We believe that we are above genetics, and that our decisions are based on our intelligence. In order to maintain our beliefs about right and wrong, good and evil, marriage, childrearing, and many other day to day issues, we insist on maintaining the myth that instinctual behavior is something the lower animals do. Humans are not so fettered. We can behave as we want, if only we have enough knowledge and determination.

I certainly don't have any intention of suggesting that humans are entirely driven by instinct, or that we don't have free will. (We'll discuss free will another time. Trust me.) However, especially with regard to sexuality, I do intend to demonstrate rather conclusively that we are not as free as we think, nor are we nearly as rational as we think. As a teaser, let's look at a very interesting trend in human reproduction.

Did you know that among American presidents, there's a striking imbalance in the male to female birth ratio? Up to George W. Bush, the presidents have had ninety sons and only sixty-three daughters. This could be considered a statistical anomaly, for the sample size is quite small. There is more, though. Royalty, aristocrats, and other members of privileged classes have also consistently shown a tendency to bear sons more than daughters. There's more still. In Peruvian spider monkeys, there's a very clear gender tendency. Among low ranked females observed in one study, all twenty one offspring were female. Among high ranked females, six of eight were male. In the middle classes, the ratio was equal. (Ridley, 117)

Still not convinced? Among many other monkeys, gender tendencies have been observed and verified. The kicker? The recorded data supports the observation that exogamy determines gender bias. In other words, the gender that leaves the group at puberty is favored among lower classes, and the one that stays is favored among higher classes. This makes sense. A lower class monkey in a male-exogamous group will be more likely to have a male, since he will be leaving anyway, and will not suffer for his low class. The high ranking females will have more female offspring, because their children will benefit from their high social rank by staying.

As a side note, this phenomenon is not unique to primates. It also happens in opossums, rats, hamsters, and coypus. Though it might be easy to write this kind of thing off to statistical anomaly if it happened in one species, and was only documented in small samples, it becomes very hard to dismiss when we are faced with multiple species, multiple studies, and repeat verification.

In the history of human culture, virtually all societies have been female exogamous, meaning that males would tend to be more common in high status pairings. On the surface, it certainly appears that this may be the case, but social scientists will be quick to raise objections. Humans have many ways of confounding this data. For instance, in societies that favor patriarchy and have invented contraception (or practice infanticide), couples will often stop reproducing after one child if it is a son. This would certainly slant the results.1

What should we say of this strange phenomenon? Since we know that humans are just highly intelligent primates, is it right for us to sweep this kind of research under the rug, insisting that we are “above that kind of thing”? If we admit the very real possibility that we are still so dominated by our genes that they somehow 'know' which gender our child should be, can we still insist that the 'War of the Sexes' and the long-running battles over societal equality are just products of faulty philosophy?

We have only begun to explore the incredibly complex subject of human sexuality. With luck, you are beginning to realize that much of the ideology you hold dear is at the very least suspect, and at the most, in danger of toppling under the weight of scientific fact. I must urge you not to jump to any conclusions just yet. We have much territory to cover before we can say that we truly understand human nature – if ever we can say such a thing.




NOTE: There is an intermediate essay that you must read in order to follow this series. You can find it here:

What Does Sugar Have To Do With Murder?!

This essay stands alone as its own topic, and so has been included in my section as a single article. In order to ensure that you don't miss a crucial step, you should read this before continuing in this series.



1If we are philosophically daring, we may ask the question, “If our intelligence is an evolutionary adaptation, and we are using it to make the decision to stop having children after a boy is born, are we really confounding nature, or are we simply obeying its mandates while feeling quite proud of our own brilliance?” I have no intention of answering this question, but it is certainly worth considering, don't you think?





Sources Used:


The Red Queen; Sex and the Evolution of Human Nature, Matt Ridley, Harper, 1993.


Human Sexuality; Personality and Social Psychological Perspectives, Craig A. Hill, Sage, 2008


The Lucifer Principle, Howard Bloom, Atlantic Monthly, 1995


The Selfish Gene, Richard Dawkins, Oxford, 1976


The Mating Mind, Geoffrey Miller, Anchor, 2000






Atheism isn't a lot like religion at all. Unless by "religion" you mean "not religion". --Ciarin

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Sources Used.....


 Now, in answer to your prior question pertaining to gene conversion and chromosomal crossover and general recombinative repair, stripped to its bare essentials, this is my intro into general recombination. This introduction of mine was prepared for other purposes, so tell me if it sounds like gibberish. The following is a course on the bare essentials of recombination that I put together:

A serious problem occurs if the DNA breaks on both strands, which will stall the replication fork. If this occurs, there exist two mechanisms to fix the problem. The first is simple, and called non-homologous end joining, in which the two ends are simply rejoined after several nucleotides on both ends are degraded from the 5' ends. This causes a slight mutation and is a rough solution. A much more accurate solution is called homologous end joining, which, in diploid organisms, makes use of the fact that there are two chromosomes with homologous DNA sequences, by which one can be used as a template for the repair of the other.

-Suppose that a double strand break occurs in a DNA sequence. If this happens, then the 5' ends of both sides will be chewed back by an exonuclease, leaving protruding 3' ends.

-The initiation of this entails that the protruding 3' ends and their single strands search for  their homologous counterparts in the other chromosome. Whenthey find each other, they form a three-strand intermediate, and this is called DNA synapsis. In it, one of the protruding 3' ends of the DNA forms base pairs with the complementary s equence on the other strand on the homologous chromosome causing the base pairs normally associated with it to flip out which are then associated with the base pairs from the other protruding three ends. This stage is presumed to be long and difficult to accomplish. Because it entails that there is a portion of sequence where the bases from one strand from one chromosome are paired with those on the other, it forms a small heteroduplex joint. After this happens, an event called branch migration begins, in which an unpaired region extends to form bonds with the complementary homologous sequence. But in the absence of any other factors, the DNA will "walk back and forth" in the three strand intermediate, there is nothing to drive the unidirectional displacement of the DNA. A protein which in bacteria is called RecA, and has a human homolog called Rad51, serves as the solution. It is an ATP-dependant protein that binds tightly to the DNA, and drives the movement of the three-stranded intermediate in just one direction, forming a nucleoprotein filament in which the RecA "spins out" a recombined DNA strand, hence acting like a treadmill, driving the DNA branch migration in one direction.


There are two principle pathways. The first is meiotic recombination. The second is repair-based recombination, and the two pathways have different outcomes. In meiosis, the genome of a diploid organism  is duplicated, and then undergoes two rounds of division. The cells that result each have one complete set of chromosomes, or half the genetic content of the cell. These then fuse during fertilization to form the gametes. Homologous chromosomes will pair, or synpase, during meiosis. Homologous chromosomes are not the same thing as sister chromatids. Sister chromosomes are copies of the same chromosome caused by replication, whereas homologous chromosomes are different copies of the same chromosome which are inherited from each parent.

     Genetic recombination occurs when a strand of genetic  material from one chromosome is broken off and attached at the homologous site on the other. In meiosis, this occurs when a double strand break in one of the two homologous chromosomes is induced by the Spo11 protein. The 5' ends of the strands are then chewed back by exonucleases. This generates the free 3' ends which can then begin strand invasion and DNA synapsis on the complementary sites on the homologous chromosomes. The DNA synapsis is mediated by the RecA protein. The free 3' ends of the two strands bind to their complementary sequences as shown:


    The Holliday Junction that forms as shown can be pulled along the DNA. After RecBCD helicase-exonuclease complex creates the free 3' ends, RecA proteins will bind to them forming nucleoprotein filaments which act as recombinases, catalyzing the invasion of the ssDNA into the homologous dsDNA.


    Chromosomal recombination occurs before the double-cell division of meiosis, when the homologous chromosomes are held tightly together. This produces a unique blueprint for the gametes. Recombination hence explains something that hitherto puzzled scientists: Why is it that offspring of the same parents do not all look alike? The difference and variety of phenotype that can be generated by the recombination of genes is testimony to the advantageous nature of recombination, and hence of the principle upon which it is built: diploid genomes.


    For recombinative repair, the 3' ends need to be created by the RecBCD complex, which is unique among the helicases in that it actually recognizes a specific sequence, called the Chi sequence, these being interspersed throughout the genome. The RecBCD acts as a helicase-exonuclease in the 5' to 3' direction, destroying DNA along ssDNA to create a protruding 5' end until it encounters the Chi sequence, at which point the DNA-binding causes a functionally induced change in the exonuclease function, also note that RecBCD is an ATP-dependant motor protein as it moves along the ssDNA. When this occurs, the RecBCD works on the other ssDNA strand, causing a protruding 3' end. RecBCD also serves to load the ATP-dependant RecA onto the protruding 3' end so that it can facilitate DNA invasive synapsis.

    The DNA synapsis leads to branch migration, in which the Holliday junctions are pulled along the DNA:

    The RuvABC complex can resolve the Holliday junction, as shown. The Holliday junction is the four strand intermediate that forms due to the pairing as shown above. After ligation, the junction can be pulled across the synapse by virtue of the RuvA/B complex (which also mounts a DNA helicase onto the strands to resolve any ssDNA structures). The branch migration is facilitated by ATP-dependant proteins, in humans called RAD51.

     RuvA and RuvB can pull the Holliday junctions along, whereas RuvC will resolve the strand by means of strand cutting:



    The Holliday junction isomerizes by rotating, at which point the joints are resolved by strand cutting:

    Hence two outcomes:

    The two outcomes of meiotic recombination as shown. Gene conversion results from SDM after incorrect base pairing due to an overt difference in the two alleles. It is for this reason that gene-conversion represents non-Mendelian inheritance. Crossovers result from standard synapsis in which the Holliday junction is resolved by isomerization. If the Watson-Crick base pairing of the two alleles is not substantive enough, then the MutS-MutL complex will destroy one strand (the MutL as usual mounting a helicase onto the DNA and the MutS binding to the muTL dimer to loop out the DNA as an endonuclease trails behind). If this is the case, then the strand that was originally from the other parent will be used as a template for the mounting of DNA Polymerase onto the strand (to be then sealed by the ligase). If this is the case, then a chunk of information that was originally from the allele of one parent will be converted into that of another. This violates a fundamental law of genetics that both parents make a precisely equal contribution to the genome of the offspring and is hence non-Mendelian inheritance (this is contrast to ). (This is again constrast to recombinative repair, where one chromosome is not changed and the other is repaired by means of using the information of the  other as a template by which the synapsis does not alter the sequence of the donor chromosome, as opposed to meiotic recombination, which does. This constitutes roughly 99% of the recombination that occurs in meiotic cells).



"Physical reality” isn’t some arbitrary demarcation. It is defined in terms of what we can systematically investigate, directly or not, by means of our senses. It is preposterous to assert that the process of systematic scientific reasoning arbitrarily excludes “non-physical explanations” because the very notion of “non-physical explanation” is contradictory.


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Hambydammit's picture

Thanks, DG!  (You're going

Thanks, DG!  (You're going in the front, under people to thank, of course)

Will incorporate this back into it after I have a chance to read through it thoroughly.  After skimming, it looks like I have a decent grasp on it.


Atheism isn't a lot like religion at all. Unless by "religion" you mean "not religion". --Ciarin

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Zombie's picture

You bastard hamby, I thought

You bastard hamby, I thought this was gonna be a good dirty read, but you had to get all sciency on us. Laughing out loud

Morte alla tyrannus et dei

  have GUN will

Kevin R Brown's picture

*blink blink*I just thought

*blink blink*

I just thought of something (Re: Sex being 'irreducibly complex')


Suppose that, within the largely algae-like substance that comprised the organisms of the early Earth, there evolved a parasitic organism that reproduced largely in the same fashion tha modern viral agents do - invading/destroying a host, transforming the host's genetic material into offspring (no doubt I'm butchering the actual process's intracacies with laymanspeek, but you know what I mean).

After a few generations, the success of this early virus eventually causes a threatened competing species of organism to develop a marvellous (well, somewhat) mutation of it's own as a psuedo-defensive mechanism: upon being invaded, the organism's genetic material fuses with that of of the parasite - so when the host bursts, offspring of both the parasite and the hosts (and/or perhaps some hybrid species?) are created.

Over successive generations, the interactions between these organisms become more cooperative and they begin to 'blend' into a singular species track.



...I haven't the faintest idea if that's even remotely close to correct. But I find it striking that someone even with my limited knowledge would be able to so easily intuit a plausible scenario for evolution to work within, using just a bit of imagination, without this Holiest of Holies for the ID crowd becoming even a marginal barrier.

"Natasha has just come up to the window from the courtyard and opened it wider so that the air may enter more freely into my room. I can see the bright green strip of grass beneath the wall, and the clear blue sky above the wall, and sunlight everywhere. Life is beautiful. Let the future generations cleanse it of all evil, oppression and violence, and enjoy it to the full."

- Leon Trotsky, Last Will & Testament
February 27, 1940