http://www.rationalresponders.com/forum/sapient/atheist_vs_theist/6927

You are as likely to have all of the complex systems of life evolve together (while at the same time supporting each other) from 'nothing' over 20 billion years as you are to get the evening newspaper (with today's current news) from a collision of an 18-wheeler carrying typewriters and a paper mill. If evolution is true, then people who believe in evolution should really stop using the word "Universe", because Universe means "single-spoken-sentence", which sounds like what God said in Genesis.

thats the most ridiculous thing Ive ever heard. Im about to repost something that I have used countless times, which shows how pathetic this argument is.

If a person says this, you might as well just walk out and leave. This most basic of errors shows that they have no understanding of basic science. Evolution is a carefully guided process.

Organisms adapt to their environment through natural selection, meaning that the environmental factors both cull the herd and remove organisms with unfavorable traits, and propagate those with favorable traits. The mechanism for this is the second rule of evolution: Evolution is brought about by genetic mutation. An organism cannot adapt to its environment per se. It is the genes that must adapt, and that process takes millions of years.

The next rule is that the determinate of what constitutes an advantage is the environment. The rest of it is really simple, Evolutionary models study this axiom because it is complex. An environment includes lots of factors like other animals, temperature, gas concentration, climate etc. etc. This axiom is the driver of evolution, the guide, Adam Smith’s invisible hand. Genetic mutation is random. It is up to the environment to nurture useful genes and ensure they get passed on, and to eliminate poor genes. This is the fundamental rule of natural selection.

This incredibly ridiculous error, to state that evolution is luck, is a confusion of genetic mutation which is luck, and evolution which is the process that selects the genes and makes sense of the randomness of mutation.

Fallacy #2 Advantageous mutation is impossible

This one is ridiculous. To understand why, a short overview of genetic mechanisms and biochemistry is necessary.

DNA is made up of polymerated strings of bases, which are nucleotides bound to sugar-phosphate backbones. DNA has two functions:
Holds the code to create various proteins from amino acids
Regulating the rate of producing proteins: By definition, one gene is a string of nucleotides that codes for one protein

The language of DNA is base-pairs. DNA is entirely comprised of four molecules. Cytosine, Guanine, Adenine and Thymine. These are the nucleotides. The nucleotides are complementary. Like magnets, they will only fit to a certain opposite. G fits with C and A fits with T (A also fits with U, Uracil, but that is an RNA base). So there are only four possible base-pairs: CG, GC, TA and AT. But these four pairs will dictate every single protein imaginable.

Chemistry has absolutely everything to do with nucleic pairing. A fits with T and C with G. They are dipolar covalents. One side is slightly positively charged, the other negative. They will bind to each other much more easily if they correspond. Trying to fit A with C or T with G is sort of like trying to force two north magnets together. This kind of error can only happen in an abundance of adenosine triphosphate. It's like protons. Have you ever wondered why they don’t repel? They smash into each other with such force that they bind (gluons). (DNA doesn’t smash into each other of course, but you get the idea. So if you have a CGAT on one string, you will of course have GCTA on the other. This is called complementary encoding, and is the basis of DNA.
There are four ways that DNA can innovate.

Intragenic mutation: Errors during mitosis can swap base-pairs around, creating new strings of bases, and a new gene
Segment Shuffling: Two different genes can recombine and form two new hybrids
Duplication error: Sometimes during mitosis, a parent cell will by accident only pass part of it’s genome to the daughter cell, thus it retains a redundant copy of a gene string. This copy is completely free to mutate based on random frequency probability.
Horizontal/vertical Transfer: During sexual reproduction, organisms exchange genes. If the organism is a diploid meaning that it’s offspring has the code of two parents, then it’s offspring will have a completely new genome, combing both parents. This is the most successful method of innovation. Or an organism, particularly prokaryotes, can actually exchange genes by means of one actually encoding a packaged gene for another, which incorporates it into the genome. This is horizontal transfer, a tool that Eukaryota do not have

There are two types of genes. Introns and exons, which have these separate functions. Exons code for proteins. Introns are mostly junk or redundant, but they flank all the exons. Sometimes they are just punctuation, dictating where a gene starts and stops, but their most important function by far is to regulate the speed of protein transcription, a mechanism we will look at it more detail later. Exons dictate how a protein will be assembled. They do this because a protein is essentially a string of amino acids or a polypeptide. Therefore, exons dictate the order of amino acids in a protein. They do this by representing each amino acid with a codon. A codon is three nucleotides. Three nucleotides make up an amino acid. There are 20 possible amino acids, but 64 possible codons, therefore, exons are highly sensitive. They are also sensitive because they are ordered very precisely. For instance, let’s look at a simple string of three codons in a gene: AGG CTT GCC. Now let’s assume that an extra base is accidentally inserted (Like a G for example). The new string would be totally different, it would look like this. GAG GCT TTG CC, so every base would be shifted down one, and the entire gene would change. This would be completely devastating. This is why DNA repair mechanisms quickly target such errors.
On the other hand, Introns, which are not so sensitive or precisely executed, or are sometimes just junk or redundant, mutate based solely on random frequency. As there are 44 codons that don't correspond to an amino acid, these are used in introns. Therefore, the next axiom of evolution is that evolution is driven by the Introns. Obviously it is more complicated, Introns can become exons during shuffling/shifting, and exons can become Introns, and sometimes exons can be mutated harmlessly, so long as the mutation changes only a tiny chunk of the gene, but this rule still applies.

Now that you understand genetic mutation mechanisms, this can be applied to how advantage mutation works.
Intron mutation can change more than just transcription rate. It can change the protein fold. So, in all likelihood an organism won’t end up with one enzyme or protein morphing into another, but an identical polypeptide folding into a new enzyme. Only exon mutation will "change" an enzyme because it will change some codons, thereby changing the protein string order. From a probability standpoint, the odds of gaining a useful mutation because you can fold a protein in a new way vastly outweigh the possibility that you can get from producing a new protein. Mutations can have chain reactions on the cycle. Same string but different protein will produce a different catalytic function therefore will change another intron somewhere else down the line, or perhaps change an exon and make a new protein which, because it is bound to the cycle, not random, will be useful. If mutations operated independently, and outside the cycle, evolution would never get off the ground.

It can be understand like this:
A useless mutation occurs: Nothing happens
A bad mutation occurs: The cell dies, or the error is targeted because it is disrupting the cycle
A good mutation occurs: A new protein, rate of transcription or fold function is made. This is useful. It alters the cycle, producing a knock on effect.

For a mutation to occur which can be preserved, junk must be turned into non-junk. It is really easy to play with the introns. The prokaryotes that are the basis of life have almost no junk DNA. It is evident that such small organisms evolved to have conservative genomes. They have useful introns. It may seem extremely unreasonable in terms of probability but DNA mutates all the time. If the shift is Duplicate error, a popular method, then the gene advantage can be conserved, because it is a redundant piece. Evolution is just mathematics. As long as a gene exists, it will fight to survive...at the chemical level there exists a ruthless primal battle in which the best of the best are constantly being selected, and the weak crushed. The only phenotype affecting genes that are conserved are the ones that affect reproductive capacity. That will cause it to be conserved and cumulatively mutated upon. This is the mathematics of evolution.
Genetic drift drives evolution. Some mutations are good, some are bad, most do nothing, but through the endless cycles, organisms evolve. The analogy I like to use is the telemarketer. About 90% of people hang up on them, but the 10% who say yes make the enterprise quite profitable.

The statement advantage mutation is impossible is a confusion of possibility and probability. Advantage mutation almost never happens…the operative word being ALMOST. But if you have mutations working at quantum speed and three billion years on your hand, your odds improve dramatically.

The knock-on effect is a good demonstrator. All enzymes do only one thing, they act as a catalyst for the body's catabolic chemical reactions. Without proteins, you would have to set yourself on fire to release enough energy to perform respiration. This is obviously not practical. All proteins lower the activation energy for a chemical reaction by providing an active site which works like a lock and key model. The chemical fits into the protein receptor and is broken into smaller molecules. Therefore, one can imagine that a different fold will mean that protein will have a different catabolic function which could offer a significant advantage if it allows an organism to synthesize a new chemical. The most effective way to do this would probably be base-pair swap exon mutation, which will only change a small chunk of an exon. Normally, the amino confirmation will predispose a protein to fold in a certain way, although this process is not understood (that would be the Levinthal Paradox). Natural selection, it seems, has selected a chemical interaction set which encourages the protein to fold, because in it's primary and secondary state, it is useless.
Protein folding is also a useful demonstrator of life's autoregulatory weirdness. They fold into elegant shapes after being translated from mRNA only for a tiny piece of it to serve as an active site. The hemoglobin molecule is the bizarre case and point. It is a colossal macromolecular protein snugly wrapping a single haemite (iron). This is somewhat akin to building a nuclear powered transformer to plug in a lamp.

There are 100 nucleic acids and 300 amino acids that exist in nature, we use only 4 and 22. The sugars and phosphates snap together to form the base backbone in the exact same way that nucleic acids bond together. From a chemical standpoint, the phosphorylate-saccharide (ribose)-nucleic acid structure is sensible. There are 100 nucleic acids and 300 amino acids that exist in nature, we use only 4 and 22. There is no reason why life could not be based on other amino acids and nucleic acids. The sugars and phosphates snap together to form the base backbone in the exact same way that nucleic acids bond together. From a chemical standpoint, the phosphorylate-saccharide (ribose)-nucleic acid structure is sensible.

We can look at the knock-on effect with respect to folding like this:
1) A small mutation changes a few codons
2) A different protein is made with a new fold
3) This catalyzes a chemical in a different fashion, most likely a new product
4) This new product has a different effect on the cell membrane receptors, which keep up the autocatalytic cycle. It causes a different command to be followed, as transcription is driven when a stimuli causes a protein to bind to the introns that flank the necessary exon.
Transgenic technology has revealed that changing a gene can start making a gene down the line do bizarre things. Why? Simple. Genes can control each other. The knock-on is established by introns controlling exons which in turn produce proteins which control introns which control exons which… you understand. If evolution operated like individual genes doing individual things, it would not get on the ground.
Knock-on effects work all across the genome. After all, what do genes do, they produce proteins, or they regulate the production of proteins. What do those proteins do? Well...everything: The big functions are of course:

-Catabolism of biochemical families (nucleotides, coenzyme factors, carbohydrates)

-Anabolism (glycogen synthesis, lipid synthesis)

-RNA synthesis control

-Ion channels and membranes (cell membranes, nerve membranes, particularly oligolipoproteins for myelin) , transport mechanisms
including inorganic transport, ion flux and carrying

-Exocrine systems and secretory pathways/chemical production

-endocrine systems and hormone control Autocatalysis

-Maintenance of cell signal transduction and energy release metabolic pathways

The thing to notice about all of these is they are all dependant on biochemical triggers. You change one thing, you change a cascade. Making a new ion channel will change the electrochemical gradient or allow a different material influx, which will affect how protein receptors bind to introns. A new ion channel could trigger a hitherto unused intron. There are so many complex factors to genetic evolution, it is not a clear cut process.

The discovery of genes was probably one of the most important in the history of science. Before genomic sequencing, the human body or indeed any organism or indeed a single celled organism seemed unbearably complex. Of course, with the advent of new molecular biology techniques that was swept away. Everything can be explained in terms of metabolic pathways building macromolecules with remarkable properties. There are only thirteen families of Biochemicals (Terpenoids, Flavanoids, Carotenoids, Polyketides, Alkaloids Peptides, Polypeptides, Amino Acids, Nucleic Acids, Steroids, Enzyme Cofactors, Carbohydrates, Lipids and Tetrapyrroles). Everything can be explained in terms of these, and the manufacture, regulation, secretion and synthesis of these…can be explained by DNA. This explains everything from simple sugar metabolism all the way to the Progenitor…the stem cell with the potential to make a human body.

Presumably when you talk about such probabilities, which I can tell were ripped from Dembski's logarithimic calculation, you make the false assumption of Irreducible compexity. I can destroy that with ease.

Irreducible Complexity is common, popular and fallacious. It was first put forth by Michael Behe and states that whereas in complex biosystems, if any single mechanism in a body function is removed, it fails to work. Thus it needs a designer. A laughable error. Every biomechanism can be broken down into simple components. We can track the evolution of an eye from simple patches of light emitting cells. Creationists like to use eyes or wings, but half a wing works fine, and might save your life if you fall out of a tree, likewise 51% of a wing will save your life from a fall from a slightly higher tree. We can see examples in nature of parachuting and gliding animals that are clearly partially and very slowly forming the systems that Behe deems Irreducible. We have fossils of birds which appear to have, half a wing or 60% of a wing. Half an eye (and there are organisms which do have half an eye) is better than no eye, and 51% of an eye might allow you to see a predator that half an eye would not. And this is how evolution works. The gradient of advantage accumulates until the “scaffolding” is no longer needed and a plethora of more advanced functions can spawn.
The organism that Behe likes to use is the bacterial flagellar motor mechanism. This device is remarkable in nature in that it is the only example outside human technology of a freely rotating axel as a means of propulsion. (Wheels on large animals really would be irreducibly complex and I suspect this is why they do not have them) It is powered by a tiny molecular motor. According to Behe, if any part were removed, the motor would stop working. Not only is this not irreducibly complex as each function works fine on its own, but we can track it back to simpler versions of it and see how it mutated. The axel bears clear resemblance to a simple mechanism used by bacteria to pump toxins into their hosts called a Type Three Secratory System (TTSS), and we can track that from simple proton pumps and ion channels.

Complex Systems do not evolve independently. You don’t see an eye in the primordial soup. A collection of simple systems accumulates more functions as these become advantageous. Darwin said in the Origin of Species: “Were it that a system could genuinely not function without the removal a mechanism, my theory would collapse completely”. So far, it holds.
There are three problems with irreducible complexity
1) Every biological function right down the level of RNA and viruses/ is self sufficient
2) Every complex system can be traced to a simple system, from photoreceptors to eyes, from ion channels to Secretion systems to flagellates and molecular motors
3) Complex systems evolve in mutual support of each other. An eye is useless without a patch of neurons to interpret it.

I can take apart one of your examples of IC immediately. I understand the Behe and the like love blood clotting:

It might be best to step back and first determine how the metabolic pathways to blood clotting work. It is a complex process indeed. At the heart of blood clotting is a substance in your blood called fibrin. Fibrin is a sticky molecule soluble in water which has the natural tendancy to form a clot. The mesh which it forms stops haemopoitic cells from escaping. Fibrin forms about 3% of the blood. However, it obviously cannot exist normally as fibrin, or it would simply block up the vessels, hence when in the blood, fibrin exists as part of a larger molecule called fibrinogen. Fibrinogen is a complex, amino-acid rich macromolecular complex, which at it’s center contains the fibrin molecule. Surrounding it are many amino acid side chains, which have a negative charge (at the pH of blood, amines and side chains always have a charge). This causes them to repel each other, thus they exist as independent molecules in the blood, without clotting.

This changes when a wound initiates the metabolic pathways known as the blood clotting cascade. A protease enzyme has to catalyze the removal of the side chains, thus exposing the fibrin. This enzyme is called thrombin. But obviously thrombin has to exist as an inactive enzyme otherwise it would simply initiate the reaction whenever. It exists as protothrombin, and has to be activated to become the catalysis enzyme. A tiny additional chain on the protothrombin fold renders it inactive. This has to be removed by another clotting serine factor, Factor X. This too, as a serine, must be activated in the same manner. And so, the blood clotting cascade has four steps more until we reach the beginning. Factor X is activated by Factor XI, which is activated by Factor IX, which is activated by Factor XII, Which is activated by the Kininogen-Kallikrein system of co-activation, which is triggered by external stimuli. This is where the process starts.

The activation of the serine cofactors is a similar process. For XI to become XIa (Activated Factor 11), a side chain must be cut removing the ionic charge, which allows it to cascade into the next step. It seems unnecessary complex, almost like an infinite regress of serine-cofactor activation steps. But it makes sense, because for every step that is taken, an exponential signal transduction increase occurs. If it was just a very short pathway, say a single cofactor triggered by external stimuli to start the thrombin conversion, then the clot would be far too small, and would take hours to form. Thus, the six-step amplification works best.

In others words, blood coagulation is a complex and beautiful process. But does that mean it is irreducible and could not have evolved? One of the key establishment requisites of Behe’s irreducible complexity is that a mechanism could not evolve by gradual evolutionary steps. But I beg to differ. The implication that he made clear in Darwin’s Black Box was that the designer would have to put all the parts together at once, otherwise it would not really be irreducible or a challenge to evolution. But unfortunately, genetic analysis of the cofactor cascade tells us otherwise. Thus we return to my previous comment about the homologous nature of the cascade.

So how could this function have evolved, and how can we trace it? Typically, when we start looking at a biomolecular function, we have a base from which to start. We never start from scratch. Only primordial chemists deal in that. This base function might be exteremly primitive, almost bound by basic laws of chemistry. For instance, when we look at the eye in all it’s glory, we see that all nine divergences that have taken their course come from a highly simplified patch of light-sensitive cells. Likewise, when we observe the fantastic complexity and variation of the Eukaroytic cell membranes, with all their complex ion channels and protein transport functions, we see that in common they are all bound a very simple chemical law known as ampipathism, the tendency of hydrophilic/phobic molecules to align in a bilayer. The membrane’s composition resembles a flagellum in molecular shape, with a long twin hydrophobic fatty acid tail and a stubby hydrophilic choline-phosphate-glycerol head.

What similar base function might we find in blood clotting? Studying the evolution of metabolic pathways is different to studying other molecular functions. The job is made significantly easier by the Autocatalytic nature of the pathways as described in my previous link. Much of the steps in coagulation work like that too. The serine proteases that form the original primitive life forms (as being detected on the long arms of chromosomes 1 and 5) were not originally designed for blood clotting, but they were there. In his book Finding Darwin’s God, Ken Miller suggests that cAMP (that’s cyclic adenosine monophosphate) would be a significant launch pad to build up the homologous set of serine cofactors that make the cascade. He’s correct here. cAMP is cellular transduction molecule that acts somewhat like a neurotransmitter, smoothing muscular tissue around vascular epithelial tissue, and inhibiting blood flow. A damaged cell, spilling all of it’s contents, would pour the cAMP out along with it. Evolution could work with that. Cellular mechanisms already possess, for unrelated reasons, white blood cells, whose adhesive nature allowed them to clump the wound

From the rudimentary system, where several factors are in place and a simple automatic system of clumping exists, a highly complex multilayered system of cascading can accumulate by two well-known evolutionary processes. One is called duplicate error from which the various homologies are formed, and the other is exon shuffling as done by spliceosomes. From the receptors point of view, we could see how the repeated duplication and slight mutation of the serine cofactors would work, for reasons not the least of which that we can track it’s paralogies. For the most part, coagulation is autocatalytic, it just needs the materials to initiate. If the progenitors are already in place, then well…all that is needed is time for the duplicative errors to occur. If we have primordial serine cofactors (we do), the rudimentary single layer is pre-existing (ie, primordial enzyme A is cleaved to make Aa, which actives the thrombin). This would initiate itself. And we can imagine the naturally selective benefits that would come from the repeated duplication of the serine, as this would make clotting more efficient.

It is in no way Irreducible. You can be sure that we would notice it in the genome if it was (as it turns out, they are strewn all over the genomes across the strata, XII is in Chromosome 5, VII is on 13, Factor VIII is on the sex chromosome etc)

Blood clotting is an example of a zymogen cascade pathway, and any metabolism generated by zymogenes can be generated by duplication and homology. This particular cascade is composed almost exclusively of serine proteases. Surely, serine protease zymogenous cascade is the worst example of "intelligent design", not because it is poor, but because the homology in this particular protein family is more obvious than any other family, kinase domains, homeodomains, Cro repressor dimers, you name it, this is the textbook example of a protein family in an obvious homology. This particular domain is so close in amino acid structure of the proteases that some of the serines are nearly indistinguishable without close scrutiny of the difference in signature sequences. (Sig sequences are tiny stretches of amino acids 10-30 amino acids long used to ID domain stretches that have diverged alot). Of course, the serines haven't exactly diverged alot. In fact, they are one of the most conserved families in the whole proteome. They are the nemesis of intelligent design, an obvious example of duplication and homology.

All life, from the humble protozoa to the strutting man, is based, without any known exception, on a linear chemical code, which holds in an ingenious fashion, all the instructions to create life in the complex forms we see around us. The composition of this chemical code is based on giant, unbranched polymers called DNA which hold the chemical instructions in a ladder-like formation. Namely, in two complementary strands which twist around each other to form an isomeric structure whose elegance is unmatched in nature. The rungs and strands of these ladder have a rigidly enforced chemical makeup which is what I shall detail now.

Each of the two strands of the ladder is made up of a string of molecules which snap together like chemical blocks. The composition of the molecule is sugar-phosphate. A phosphate is a simple, straight, branched molecule of interlinking oxygen and phosphorous. Attached to this phosphate is a radically different molecule, an aromatic sugar called deoxyribose. Traditionally, a sugar is defined as a molecule which follows the composition formula {CH2O}n. For this reason, it is also called a carbohydrate. All ring-structured sugars have a definite pattern. The inner ring is composed of a single oxygen and n Carbon atoms which are arranged in a circular, single-bonded pattern. Each carbon atom in the inner ring has attached to it one Hydrogen atom, and one Hydroxyl group (OH). All of the carbon atoms have this, that is, except one. Attached to one of the carbon atoms in every sugar is either a ketone or an aldehyde. Both of these are small, simple chemical groups which radically alter the sugar’s chemical property.

A ketone is very simple. It is a carbon with a double covalent bond to an oxygen. Because a carbon has a valency of four, there are two open spaces in this molecule for bonding, which is how it attaches to the ring of the sugar. An aldehyde is more or less the same, except it has a hydrogen attached to it, leaving only one free space. The sugar in DNA has an aldehyde.

The sugar in question in DNA, which is called deoxyribose, has all of these properties except one. Instead of it’s normal derivative sugar ribose, it is missing a hydroxyl group (specifically at the second carbon atom in the ring). This will become important later on.

The structure of the strands of DNA therefore, is a repeating polymer of a sugar ring linked to a phosphate linked to a sugar ring linked to a phosphate and so on. For purposes of keeping the integrity of the ladder, the other strand in the DNA molecule, called the complementary strand, has the sugar-phosphate aligned in the opposing direction.

And what of the rungs of the ladder? Well, that is quite special. It is the rungs of the ladder which hold the information, and it is the order of the rungs of the ladder which determine this information. Attached to each sugar-phosphate on both strands of the ladder is a molecule called a base. The language of DNA is made up of four bases. You may recognize their names. They are adenine, guanine, cytosine and thymine. Like sugars, all of the bases are ring structured. But they are a radically different class of molecule. Sugars are merely carbohydrates. But bases, in addition to hydrogen, carbon and oxygen they have one more element to their mix. Nitrogen.

There are many, many bases in nature, almost 100, but DNA uses only four. And within those four are two quite different classes of bases. The purines are heterocyclic, meaning that they are actually composed of two rings, not one. Many notable molecules are purines (like caffeine) and their importance extends beyond their part in DNA.

(Irrelevant but interesting side note. Methylation of some purine bases can produce free radical bases like hypoxanthine. These have a direct link to cancer and can damage healthy DNA)

Out of the four bases present in DNA, two of them are purines, adenine and guanine, which henceforth shall be referred to as A and G, and the other two referred to as C and T.

What of the others? They are a different class of base called pyrimidines. These are simpler than purines, and have a familiar single-ring structure. The pyrimidines are the class of molecule under which C and T fall.

What is the importance of the purine/pyrimidine relationship? DNA is based on a molecular relationship called complementation. Recall that DNA is made up of two strands. Each strand is made up of alternating sugar-phosphate, and the two strands face opposite directions (i.e one strand is sugar-phosphate-sugar-phosphate and the other strand in phosphate-sugar-phosphate-sugar).

Each sugar-phosphate has one base attached to it. This produces a special molecule which is called a nucleotide. What is the set of nucleotides above classed as? They are called Deoxyribonucleic acid, otherwise known as DNA.

Because the structure of DNA is held in complementation, each base has a pair. This is where the purine/pyrimidine relationship becomes important. You cannot force two North magnets together, and in the same way, the DNA code follows strict chemical rules. A will only fit with T, and C only with G.

In this way, we can start to see how the DNA ladder is formed. Each step is composed of not one rung, but two. Each side has half a rung attached to it, and the other half of the rung is determined by the pre-existing chemical composition. This is exactly how DNA replicates itself. The process is called templated polymerization. Imagine half a DNA molecule, which only has one strand. Swarming around this strand are many free nucleotides. They will automatically attach themselves to the bases on the pre-existing strand, and the complementary strand will start to take shape. If a single strand reads ATTCGGA then the complementary strand will read TAAGCCT. Although each strand keeps it’s chemical integrity through very strong covalent bonds, the two strands (who connect to each other via the bases or rungs) are held to each other by weak hydrogen bonds. This allows the two strands to peel apart and snap together with ease, which allows repeated polymerization and replication. In the lab, we can replicate this process through a technique called PCR or polymerase chain reaction.

This is the basic chemistry behind DNA, but leaves the more important question unanswered. How does this translate into the information needed to create life? How does the order of bases along a string translate into the information needed to build a cell?

DNA is a linear chemical code. It faithfully represents another class of information in a linear fashion. It has many uses which will be detailed, but any cellular biologist will immediately give you one answer: DNA holds the code to make protein.

Proteins are radically different to nucleotides. They are also composed of massive, unbranched polymers. The language of protein is composed of linked amino acid subunits. In all of life, there are 22 known amino acids and a protein is determined by the order of it’s amino acid string. This is how DNA represents proteins faithfully. The order in which DNA bases are aligned on a string is a direct representation of the order of amino acids on a protein. But how does a code of four chemicals represent an alphabet of 22?

The answer lies in the correct way DNA is read. One amino acid is represented by a specific order of three amino acids. This information structure, where DNA is grouped in triplets, is called a codon. As it is groups of three based on four possibilities, there are 64 codons and there are multiple codons which can correspond to a single amino acid. In fact, most amino acids can be represented by four codons. For instance, Serine can be read as TCT, TCA, TCG or TCC.

The definition of one gene is the length of DNA which represents one protein. A gene tends to be roughly 1,000 base pairs long, the size of the average protein. The process by which information from DNA is turned into protein is called transcription and translation. This process is very complex in its trigger mechanisms and enzymatic control. A simplified version will suffice. Recall that double-helixes can peel apart to expose the strands for replication. This is the foundation of protein synthesis. The DNA first needs to be translated into a slightly different language called RNA.

RNA is also based on sugar-phosphate and bases. It is nearly identical to DNA except for some critical differences. The sugar in the RNA backbone is standard Ribose, not deoxyribose (hence the acronym). This causes it to have a much weaker backbone than DNA. Also, one of the bases is replaced. RNA contains C, G, and A like DNA. But instead of thymine it contains another (very similar) base in it’s place- Uracil, denoted by the letter U. Isomerically, it is much less elegant than DNA. It is single stranded, not double, and because it’s backbone is much weaker, it tends to fold on itself. For instance, an AAAA section will associate with a UUUU section. Far from the beautiful twisting symmetry found in DNA, RNA is an odd, crooked molecule.

For DNA, nothing complex is required. A set of reactions that reads DNA is based on literally copying it. The key thing about DNA is that the nucleotides literally represent amino acids. One codon is identical to an amino acid. This is translation/transcription. I'll go through it step by step again.

1. A stimulus from the cell membrane causes proteins to bind to the introns flanking the necessary exon, this causes the string to unwind. This is initiated by transcriptase enzymes
2. Once unwound, the string splits
3. Through templated polymerization initiated by polymerase enzymes, free bases attach to the complementary string, producing the identical string (that which is precisely identical to the protein in question in terms of codon order), which is then tidied up using spliceosomes and ligases, enzymes that cut through the introns and glue the exons together to make the complete string.
4. The Free bases are RNA bases and attach to form the protein-identical RNA base. The reason for this is that a ribosome cannot read DNA, it must be converted into RNA. The only difference is that it has ribose instead of deoxyribose and uracil instead of thymine, but since nothing else can read thymine, that is an important difference. This string is called mRNA which is ejected from the nucleus.
5. tRNA strings which represent one amino acid bind to their corresponding amino acids on one end. On the other end they have an anticodon, which represents the base string identical to the amino acid.
6. The mRNA is captured by a ribosome, a giant macromolecular protein. The mRNA is lined up along it. The anticodon on the tRNA automatically binds to the codons on the mRNA. This forces all the amino acids to line up. They thread together automatically, which causes the now unnecessary tRNAs to detach and leave the ribosome. When the protein is finished, it is automatically detached.

The definition of one gene is the length of DNA which represents one protein. A gene tends to be roughly 1,000 base pairs long, the size of the average protein. The process by which information from DNA is turned into protein is called transcription and translation. This process is very complex in its trigger mechanisms and enzymatic control. A simplified version will suffice. Recall that double-helixes can peel apart to expose the strands for replication. This is the foundation of protein synthesis. The DNA first needs to be translated into a slightly different language called RNA.

RNA is also based on sugar-phosphate and bases. It is nearly identical to DNA except for some critical differences. The sugar in the RNA backbone is standard Ribose, not deoxyribose (hence the acronym). This causes it to have a much weaker backbone than DNA. Also, one of the bases is replaced. RNA contains C, G, and A like DNA. But instead of thymine it contains another (very similar) base in it’s place- Uracil, denoted by the letter U. Isomerically, it is much less elegant than DNA. It is single stranded, not double, and because it’s backbone is much weaker, it tends to fold on itself. For instance, an AAAA section will associate with a UUUU section. Far from the beautiful twisting symmetry found in DNA, RNA is an odd, crooked molecule.

Nonetheless, it is a critical medium to protein synthesis and a key material in macromolecular cellular structures. The cell’s protein synthesis mechanisms, which I will go into in more detail, cannot read the language of DNA. Therefore, it must be translated into a slightly different format which can be processed. This interface string of RNA, the medium between DNA and protein, is called mRNA, or messenger RNA. It is the template which serves to manufacture a protein.

When we look at a cell under a microscope, any cell that we wish to examine, it bears many different things. Strange swirling little organelles and beating cilia and loopy strands of DNA. They are very diverse, but there is one thing they all have, without any exceptions whatsoever. Under a microscope, it appears to be many tiny black granules, little spherical studdings that are strewn all over the cytoplasm.

However, using electron microscopy and X-Ray crystallography, we can see that these little black balls, are first of all, not black (false colour imaging) and second of all, they are not little balls, they are colossal macromolecular structures, extremely complex and interwoven, beautiful little machines. Under a Scanning Electron Micrograph, the power of the “little black balls” becomes humbling. These little devices are called ribosomes. They are composed 75% of twisting strands of protein, and 25% of a form of RNA called rRNA or ribosomal RNA. This RNA is not coding RNA, it holds no genetic information in it’s molecules, rather it is structural, the scaffolding for a miraculous little device.

The ribosome is a protein synthesizing complex, trundling along in the fluid medium of the cell, and capturing the raw materials and information to make the protein and then, remarkably, stitching together a fully functional protein based on these ingredients.

The raw materials are already in the cell, they are amino acids. The information to synthesize the amino acids is also in the cell, in the form of the mRNA strand (which is ejected from the nucleus). Yet the ribosome does not just scoop up amino acids wherever it finds them. They are brought into the ribosome, and arranged in the correct order on the mRNA by another class of RNA molecule called transfer RNA or tRNA.

Amino acids cannot be synthesized off the mRNA template alone. The languages are too different. There has to be a third medium to read the information. This is where the tRNA comes in. It has the capability to read both sets. tRNAs are special molecules. They are also composed of RNA, yet on one end of them they have a binding site which is unique to each amino acid. Due to the triplet nature of the reading of DNA, multiple types of tRNA molecule can correspond to a single amino acid.

The other end of the tRNA has three base pairs, which will correspond to the amino acid to which it binds. However, this relationship is special. For the triplet on the tRNA does not correspond to the amino acid with the parallel relationship the acid will share with mRNA. Rather, the triplet is the precise mirror image of the amino acid codon. For this reason, it is called an anticodon. This concept is relatively easy to grasp. If an amino acid is represented by AGG on the mRNA string, the tRNA to which it binds will have UCC tagged to it.

From here it is easy to see how the process unfolds. The ribosome is unbearably complex, a colossal protein/ RNA complex which is the subject of countless research papers. It is divided into domains based on the subunits which compose it, and the genetic control switches which produce the rRNA and protein to make and assemble it, as well as control of the anabolic processes which synthesize it from macromolecules, could not possibly be described in this very short introduction. For now, suffice it to say that the ribosome is arranged in two large domains with slots to hold the molecules in place. As it moves through the cell, it captures the free-floating information in the form of the mRNA and the tRNAs now bound to specific amino acids. In the smaller of the two domains, the mRNA strand is threaded through a slot-like mechanism similar to a conveyer belt. In the larger domain, there are accommodating slits which house the tRNAs.

This is where the factory process unfolds. The tRNA anticodon can recognize its counterpart codon on the mRNA string, and thus they will line up in order automatically (note: To prevent tRNA insertion into the wrong place, and to ensure they line up strictly in order, there is a complex cascade of enzymatic control barriers and mechanisms whose details need not be mentioned here).

Once the tRNAs are lined up in the correct order as dictated by the information held by the messenger string, the amino acids atop the tRNA are now in the correct order, which was the desired state of affairs to begin with. They are stitched together inside the ribosome. Once two amino acids have been stitched together, the tRNAs holding it are no longer needed, and they are enzymatically broken from their acid, and ejected from the ribosome. One by one, the tRNAs stream out of the ribosome until the protein is finished.

At this point, the work of the original gene which contained the information to make the product is finished. However, the processes which I shall detail next are, like every other process, controlled by genes. There is no function in the whole of biology which does not have genetic control mechanisms.

The protein is now correctly assembled, at very least in terms of having the correct order of amino acids. However, the actual product is far from complete. It is only in what we call the primary structure. In terms of chemical composition it is completely correct, but in terms of isometrics and structure, it is little more than a string of chemical compounds.

The true magic begins almost immediately after the protein is synthesized. It begins to twist…

A protein is not subdivided merely by it’s amino acid. It is grouped into large subunits called polypeptides, regional stretches of protein subunit roughly 100 amino acids long. In this way we can see that massive proteins (>1000 amino acids) are not only defined by their individual, but ultimately, the order of different units created by smaller strings of amino acids within the complex. The protein transforms into it’s secondary structure by folding at the kinks between the subunits. The shape, therefore, of a protein is directly determined by it’s chemical sequence. The folding becomes further intricate during progression to tertiary structure when the folds between individual units take shape. Finally, the protein reaches it’s quaternary structure or it’s native state, with the intricate system of folds.

New information is gained by a mutatory mechanism that satisfies two requisites at once. The size of the genome in terms of bases grows, and the diversity of the genome grows. A special mutation known as duplicate error, where a spliceosome makes a mistake, and during mitosis a duplication ends up with the progenitor cell retaining an extra part of the genome. This new part is redundant, and thus free to mutate based on random frequency. This mechanism is critical to evolution, and produces two genetic flows without which evolution would not be possible. These are paralogs and orthologs. Across the vast diversity of life, the majority of genes share a near-identical similarity to another, with a very similiar job. These are grouped together in large gene families. All the gene families have a lineage that stretches back four billion years.

On this subject, in an article not displayed here, this is what I wrote:

DNA genomes are extremely redundant. 91% of the human genome is redundant, if you are interested. So changing one copy will add new information. Because most of the time the polymerization works out fine. Imagine it like a library. There is only one copy of each book. You remove one book and replace it with a different, new book. Are you adding information? No. You are changing information. This is the crux of the creationist argument. But imagine you have twelve copies of each book. You replace one copy of one book with a different, new book. Now you are adding new information because the pre-existing information is still there in the form of 11 other books.

Evolution is dependent on homologous sets of genes called orthologs and paralogs. Genes in multiple organisms that obviously descended from the same common ancestor (anyone who bothers should check the amino acid tracking branching tree of hemoglobin evolution as an example) are called orthologs, while genes which occurred as the result of mutation descended from a single gene (thereby producing two or more new genes) are called paralogs. Both of these are called homologs.

I also wrote some more on DNA origin here:

Protein assemblage too, is not chance. We would not assume that favorable formations of protein assemblage whereby the natural quaternery state would arise is affixed the same probability as a useless denatured amino acid string. That is ridiculous, and has been debunked by the Miller-Urey experiment. Insofar as the nucleic acids and proteins of cellular mechanisms are primary life (ie they are capable of self-assembly), they undergo their own natural selection. This was demonstrated as far back as 1936 when Alexander Oparin showed that in an anoxic atmosphere, organic molecular structures of the basic primary state would combine to construct elaborate complex macromolecular giants which themselves were capable of reassembly.

After all, what makes a protein successful? A protein is just a catalyst, whose amino acid configuration allows it to fold up in a quaternery state where it serves as multiple active sites. Only polypeptides with certain strings of amino acids acheive this state. But, as the macromolecular covalescence occurs, might protein undergo it's own natural selection? Where proteins that "work" would survive in place of the denaturing ones?

And then in 1961, Joan Oro, A spanish biochemist, cracked the adenine conjecture when he showed that the prebiotic nucleotide can assemble from hydrogen cyanide. Upon examination of comet traces, he concluded that comet fragments could have easily brought organic molecules to Earth. This in effect would merge Abiogenesis with panspermia except without the space aliens nonsense. His research paved the way for several more experiments, where the prebiotic synthesis of the other bases, thymine, guanine and cytosine, were demonstrated.

"2. Irregardless of your belief system..."

 DAMN IT!!!!

 'Irregardless' is an erroneous word that, etymologically, means the exact opposite of what it is used to express.  One might call it, uh, an imaginary word.

First as you can see, I am a theist. However I am also a Physicist.

This is actually cosmic evolution. but anyway this assumes that the Big Bang produced all the planets all at once. It did not. It produced Hydrogen, which collapsed under gravity to form stars.  Stars used nuclear fusion to form Helium and Carbon. The stars then supernova'd creating enough heat an pressure to form the heavier elements. The elements collapsed under their gravity to form the planet you are standing on right now. 

The spin of the planets and the galaxies depends on many things. Google Kepler's laws or take an approiate physics course such as Analytical mechanics.

Their are several things wrong with this statement. First stars supernova far away from our planet. Sometimes hundreds of thousands even millions of light years away. It then takes hundreds of thousand or even millions of years for the light to reach us. So if stars supernova'd recently, we won't see it for another million years or so.

Please look at Kepler's laws

[sarcasm] Yep. Haven't heard that one before.[/sarcasm]

I did. Just like I've read your same post written by others over the last 9 days.

I prefer the quote followed by response format.

Sooo, is searching the forums and thread topics for previously posted material a subjective exercise? Or is it objectively common courtesy?

I appologize in advance if you are offended by any of my answers and comments. Please do not take them personally. I enjoy healthy dialogue and debate about these things because I'm curious and really, really want to know. I welcome you back sincerly to the forums so we may talk. Sometimes it will/may be a three-some conversation including your god and/or it can/may be a conversation between you and I and everyone here. Either way, glad you came by to talk.

Please do come back and take the time to address each of my questions and comments. I would really appreciate knowing what your thoughts and/or answers might be concerning them. Please, if you can, keep them simple and short. I'm not the brightest star in the sky, if you know what I mean (but I'm working on it), so it would be great if they were comprehensive and challenged my current beliefs into reconsideration in a way that I can understand.

I really do want answers. That is why I am here and participating. Also, many of the people here are extremely intelligent and thoughtful and have very good answers to a lot of very good questions. They have welcomed me and everyone here regardless of what our beliefs may or may not be, so I really appreciate the education I recieve here. Sometimes, I can feel my brain grow when I read and read and read. I am so grateful for that. They are funny here too. Also, I enjoy their company. I encourage and welcome you to find out for yourself.

I'll leave all the scientific stuff to others here. They are far more superiour in these areas and have addressed all your issues many times in the past in this very forum and are still kind enough to inform, educate and explain. I am not educated in any scientific field and they are far more patient and kinder than I.

However, as humans, they may be offended. I know I was. I will try not to hold it against you unless you truly deserve it.

I don't usually answer posts like yours. Fortunatly for me, there are others here are far more articulate and intelligent dealing with lies (I appreciate that) but I have to because I am so worried and scared right now.

I'll try to keep my answers short. I'm a pretty simple person. I can only speak for myself. It would be wise for you to consider everyone's comments individually.

Please don't take my answers personally. I'm just being frank and have answered/commented on those issues in the past so my answers have been edited down for efficency (I have poor typing skills so it would be in in our interest if we both can understand them).

But understand you have insulted me. I am offended that you would even suggest these lies to me. It's hurtful that you would treat me like I'm stupid or something. And it's mean.

Not only that, I am horrified that you ended your propaganda and lies with a quote from Hitler. Just Horrified. I don't think that was just a coincidence and I am afraid it might be more than that.

Please tell me this is a joke, because this is scaring the shit out of me. I am so horrirfied and terrified my hands are shaking.

Do not take my answers personally. Do understand, it was very difficult to not be emotional under the circumstances. My answers don't matter much anyway but you are terrifying me and I have to ask you to please be more sentitive. Posting lies and then posting a strategy for population control from Hitler has me almost in tears. I know it's ironic, but it's not funny at all.

Like I said, please don't take my answers personally. I am trying my best.

Okay!

I agree. My answer to, "Does God Exist?" is: We don't know. But your god doesn't exist.

I agree. And? so?

I agree. And? so?

I agree. And? so?

No. That is not what atheists are. I don't believe in your god. That is not a faith. I also don't believe in Santa Clause. What would you call the faith of that?