Well, I am a trained molecular biologist, and really nothing in this post makes any sense whatsoever. What an idiot. I hope this helps. Firstly:

Doesn't he know these are two different biopolymers?

Where did he get the ex nihilo from? He should read what I wrote on the development of biomolecular structures An example I provided:

Blood Clotting (along with molecular flagella motors and immune system functions) is claimed Irreducible by the biochemist Michael J Behe, a major proponent of intelligent design. Upon receiving word of this, I was so astonished that a man with such credentials could swallow something so absurd, that I set about immediately showing that coagulation/fibrinolysis is not so, definitely not Irreducible as claimed by Behe.

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 zymogene cascade pathway, and any metabolism generated by zymogens 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 a lot). 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. The Allosteric control mechanisms (serines work on a phosphorylation switch-gated amplification control mechanism based on a positive ligand/substrate feedback) could have easily evolved in lockstep with genetic duplication. The basics of enzyme kinetics dictate it.

We have 16,000 homology catalogues, Endogenous Retroviral insertions, and Mitochondrial DNA transfers. This relationship is extremely obvious, and it is not one, it is tens of thousands of homologies which clearly diverge as separation widens and close as it narrows, as indicated by time length separation. This test will come up on any protein domain I pick. It clearly indicates that life began a primordial genome, and as the genome duplicated, parts diverged and it expanded thusly. Genetic duplication error and polyploids are set in stone fact, and no geneticist would say otherwise. I can even watch gene duplication myself, using a microarray, although I hardly think it is worth the trouble. Using decoders, microarrays, and homology databases, geneticists have now catalogued evolutionary relationships between vast swaths of life, and the effects of these changes.

The existence of paralogies of genetics across the families in the proteome, even diverged as far as separations between the three domains themselves, and the fact that amino acid tracking reveals this to narrow as the organisms in question become more closely related (a fact which is reinforced by advanced radiometry) can only be possible via repeated duplication and divergence of genes, thusly bearing gene families which in turn branched out depending on the survival requisites of the organism and location, the lack of originality in the proteome, especially the vertebrae proteome, which can be explained entirely in terms of domain shuffling and protein string recombination can only be explained by origin from a common descent, a primordial genome who bore only the survival requisites for the simplest of life. What this genome may have looked like is mysterious, but insight into a small bacteria called Mycoplasm genitalium can give us the answer, when computationally recombined with cross-references of genes exclusive to archae, eubacteria and eukaryotes (Excluding ESP proteins of course) we arrive at an answer of roughly 200 genes dedicated to basic metabolic and structural proteins, rRNAs and mitosis control gates. Ad it is from this humble beginning that life evolved. A fact which is correlated 100% by genomic/proteomic analysis and ortholog/paralog/xenolog tracking.

Quite simply, molecular genetics tracking, ERVs and mtDNA, in addition to computational searches for paralogies across the spectrum, leads us inevitably to the conclusion that the whole swath of life arose from a single, simple, primordial cell.

I will now turn to a complex explanation of homologous amino acid tracking, which is very hard, so I will not bother to explain it to non-scientists. Sorry.

Homologous tracking can be distinguished from noise mutations from distinct signature sequences on the protein. For instance, a protein which is common to the whole of life Called Elongation factor-Tu or EF-Tu is a control mechanism for tRNA at the ribosomal junction with the mRNA string for protein synthesis. A critical control mechanism for m/tRNA match, the EF-Tu is a GTPase protein with multiple domains. The EF-Tu holds the tRNA as masked in position for translation via bonding to the mRNA. The hydrolysis of the GTP on the EF-Tu induces a major conformational change, since it has a crucial alpha-helix called the switch helix which can, due to the crucial positions of polar amino acid, switch between two crucial domains. The position of the switch helix depends on the hydrolysis of GTP. When the GTP is bound to EF-Tu, the switch helix is locked in place, which means that the tRNA is still masked. When the GTP is hydrolyzed in GDP, the switch helix opens the domain latch, releasing the tRNA.

In this way we can see how a small conformational change can amplify the signal and induce a major movement change in the conformation of the protein, such is how precise the protein's moving parts are. They are the most well-engineered devices in nature (and much more complex then any of man's devices)

So when we examine the vast swath of EF-Tu domains across the spectrum of life, the switch/latch sequences are almost unchanged, such is the precision of the protein (this effect is also present in catalysts, since the replacing of a single aspartate with a glycine in the binding site of aspartate transcarbamylase is enough to shift the position of the transition inducing carboxylate by the radius of a hydrogen atom, which is enough to decrease the enzymatic activity by a thousand fold).

Therefore, then, even with all the noise mutations, the sig sequences do not change in billions of years. But it is the noise we are concerned with, since the indication from the divergence of the same domains, while retaining the sig domains, clearly indicate that they arose from a single common ancestor. Domain divergence is not possible if we assume design or creation.

Here's a picture to help

http://bass.bio.uci.edu/~hudel/bs99a/lecture25/tugdp_for_bs99a.gif

The switch helix on EF-Tu is distinct, it is orange in this picture. Notice how it can swing between the two domains, the one on the bottom right, and on the top right. The helix, as well as the receptor domains and the GTP-binding site, the Allosteric ligand control system and tRNA site will change very little throughout the spectrum of life. Everything else freely mutates on the basis of random frequency, and in a precise rate and order that is easily predicted and shown by molecular biologists. This noise mutation is excellent evidence for evolution, because it clearly indicates that all EF-Tu holding species have a common ancestor (EF-Tu is a prokaryotic control protein, not present in Eukaryotes). This is checked against the most highly conserved proteins, because these indicate with distinction evolutionary relationships. Some proteins and gene sequences are so common, so vital, that they literally do not change at all. For example, a protein critical to all Eukaryotic life, the histone octamer around which DNA is wound to package chromatin for sequestering inside the nucleolus, is so highly conserved that the difference between the histone octamer for the human being and the potted pea plant(which are separated by over 1.5 billion years) differs in less than 1% of amino acids.

And to generate new creative domains for the creation of new phenotypes for organisms, we turn to the following.

It is about duplicative mutations, followed by recombinative mutations, or shuffling mutations. For instance, 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.

Many people say that mutations are always destructive or deletrious, or "remove information" or that DNA repair blocks mutation. Nonsense. I've studied DNA repair for a large portion of my career, and I assure you that it is not a limiting factor. THe enzymatic lockstep (it is controlled by ribosomal machines at the site of transcription) is operated on a feedback loop that only detects harmful mutations. Like I said, evolution is mostly about recombinative and shuffling and duplication mutations. DNA repair is a system to fix point mutations, which are mostly harmful, and when harmful, the enzymatic response performs , BER, MMR or NER (Base-excision, Nucleotide excision or mismatch repair) to correct the nucleotide incorrect arrangement (as it will be detected by the ribosomal transcription checkers). This is why nearly all divergences are preceded by duplication (homology)

there is almost nothing original in the vertebrae genome. It is the result of multiple whole-global duplications throughout evolution. Even in humans, the proteome contains only 7% vertebrae-specific proteins. The only place we really seem to have any originality is in domain shuffling (Im pretty sure that the human tyrpsin can bind to at least 18 domains, while in drosophilia it's only 5). As I said about protein structure, much of the innovation merely comes from rearrangement of subunits, which is beneficial in terms of the shuffling mutation quite often.

An excellent example of how evolutionary mechanisms can create novel protein combinations which can give survival benefits to the carrier organisms is found in a pair of the most critical classes of proteins in the whole of life: Kinases and phosphotases. I would go through exactly what these do, but that will take hours, so instead I will just explain it in short summary, which will sound like jargon, so here goes:

Kinases are protein phosphorylating class of signal transductors which control a large amount of proteins and amplify many, many signals, also acting as signal-integrating proteins by anchoring to the extracellular matrix junction and relaying signals from the membrane to the Endoplasmic reticulum and the nucleus. Instead of a ligand reciprocal/cooperative Allosteric binding site to control the action of the protein in question, a certain side chain (always a threonine, serine or tyrosine) is phosphorylated, which activates or deactivates the protein. The cyclic nature of kinase loop functions is very similar to that of GTPases. The largest superfamily of kinase is a simple monodomainal kinase called the Ras protein. As evolutionary mechanisms took course and organisms became more complex, a wider range of transductors became required, which evolve in lockstep with other evolving functions, a process called coevolution. This has been indicated by the fact that the Ras like domain has since become integrated into totally different proteins, and created entire classes of kinases simply by joining the Ras to many other domains throughout the course of evolution to create novel protein combinations. The branching of various kinase families that results from this is fully consistent with molecular clock tracking of the divergence rate of the amino acids (recall noise mutations). Which means whole families of kinases have been generated at different times in the evolutionary process by duplication and divergence. We now have many, many families of kinases including Cdc7, PDGF receptors, TGF-Beta receptors, Ca2+ dependent kinase, CdK integrators (which include a large range of Cdk including Cdk2 and Cdk3), Src kinases, KSS1, the list goes on and on.

This is just a small example of how evolutionary mechanisms can generate huge numbers of novel proteins simply by recombination and duplication. The lack of originality or "design" in the kinase family, as well as the prescence of Ras in every kinase and the underlying signature sequence is clear evidence for a primordial kinase upon which the whole family was built, simply by the course of time and natural selection.

This is the tree for the relationship between some kinase families:
http://bmc.ub.uni-potsdam.de/1471-213X-5-8/1471-213X-5-8-2.jpg
As we can see, this short stretch has signature sequences, exactly like the test for haemoglobin

These are divergences found in an identical protein domain confirmed exactly by molecular clock tracking against the known divergence rate of the domain and the orthologous seperation of these two species. If (as the creationist claim) these species were created within days of each other, or had no common ancestor, this divergence would not exist. This is the same domain for each animal, which I took the liberty of sequencing myself. Because I can.

Orthologous Divergence of the haemoglobin chain of various vertebrae correlated by molecular tracking, as shown by a commonly repeated molecular clock test, that of haemoglobin. As an oxygen-binding protein, haemoglobins are present in all multicellular Eukaryotes. It is, as well as an excellent example of homology due to the fact that it is arrayed in batches and is part of a superfamily of oxygen-binding proteins, very easy to test with the molecular clock, to see the rate of divergence on noise mutations. The very fact that we get positives on the molecular clock is enough to disprove the notion of design, seeing as the time/divergence relationship is only possible via evolution of the protein batch via duplication and homology and divergence.

Percentage divergence in amino acids between conserved domain of haemoglobin

Human/Lamprey (divergence: 550 million years ago) 35%

Human /Shark (Divergence: 520 million years) 51%

Human/tuna fish (450 million years) 55%

Human/frog (350 million years) 56%

Human/chicken (320 million years) 70%

Human/lizard (270 million years) 77%

Bird/Crocodile (220 million years) 76%

Human/Kangaroo (170 million years) 81%

Human/Sloth/Mouse/Elephant/Rabbit/Pig/Sheep/Whale/Cat/Dog/rat

All between 150 and 50 million years, all 80-85% related in this domain

Human/orangutang (10 million years) 98%

and finally...human/chimp (7 million years) 100%

Regarding his examples on the interaction between abiotic and biotic factors of evolutionary process, and the especially amusing comment about biological structures "deciding" to do things, it reveals idiocy of the highest degree. The author understands truly nothing, nothing of evolution. By the way, all metabolic pathways develop due to modular domain protein recombination. Anyone educated in Enzyme Kinetics will know this. It shows nonexistent understanding of evo-devo.

It is not merely that a functional trait becomes more pronounced in its concentration in the pool of organisms due to the survival benefit it offers, and hence the increased reproduction, (which in turn leads to a greater increase in concentration of the trait with every generation. So, between F-1, F-2, F-4 etc, there is a calculable rate at which the trait will proliferate in the population. However, ecology is not my field, so I cannot discourse on that). But the other factor which we must look at is that the new phenotype becomes much more pronounced as a trait with the move from F-1 to F-2 and so on, until the accumulation develops into a fully fledged and distinct physiological and morphological change in the organism via speciative mechanisms we will be examining later. A wing does not spring forth overnight. Its development is gradual, perhaps the exaptation recombination from pre-existing functions (Again, zoology, not being my field, I cannot comment on this. However, I will comment on the evolution of the wing as a genetic process in the next essay). There are also physiological and natural checks on the refinement of a single morphological trait, the physiological being simply that after enough refinement, increase in size etc, the continuation of growth is no longer advantageous, and the natural being, as we shall soon see, that should the refinement of trait provide the organism sample in question with such a massive advantage that it begins to overpopulate, then crashes and burns. We shall explore this later.

We must remember that this process is not occurring with one but hundreds of trillions of organisms over tens of millions of years. There will be hundreds of thousands of animals who are all refining the same trait. But mutation is random. How is this possible? The answer is that mutation is random, but the process which forces it in one direction, ie natural selection, is not. All variable traits begin in the most humble fashion: From a single progeny. This single organism holds the key to the continuation of trait. If the advantageous mutation (as it must be) is contained within the DNA of a gamete, then the mutation in question will be copied into every cell of the progeny in utero (there are mechanisms to stop deleterious mutations from entering the equation, and we shall study these in the next essay). As generations accumulate, from F-1 to F-100 to F-100,000, we shall see that presuming the trait in question is advantageous enough to warrant survival advantage to the organisms carrying it such that they will have a reproductive advantage, then this trait will accumulate, and then we will have vast numbers of organisms carrying it. But I return to the original question: How does it progress from there? For how can mutations act in synchronicity when they are random? The answer is that they do not. The environment, the factors which put pressure on the population, simply force the continued development of trait in one direction, since the whole population is experiencing the same natural pressures. When the population is not experiencing the same pressure, that is when, as we shall see soon, a phylogenic break-off may occur.

Now, the recombination of genetic material can extend far above the level of single proteins or domains. Indeed, enormous chunks of genetic material may be recombined. Hence, when examining homologies, we can examine relationships that go up to the quaternary level, caused by large order duplications or recombination. Indeed, we are often tempted to think of evolutionary increment as “adding parts” or something of that like. This is a very primitive design-style worldview of looking at evolution. Indeed, the process can add parts and delete parts via these mechanisms, but this is a rare occurrence (begging the question of what a single “part” is anyway). Many complex biomolecular structures can generated by the recombination of pre-existing structures into a new role, which is a rapid-order mutation, instead of incrementation to generate the whole structure in question, incrementing generates some of the underlying mechanisms of the structure in question, and then these underlying protein structures may recombine to rapidly form the product structure. If only two or three pre-existing major components are required to generate the new and supposedly “irreducible” function, then it can be generated by what is called exaptation which is, as described, a process by which major structures (which may have no relevance per se to the function which they recombine to form) recombine and create something, which, when broken down into its fundamental constituents, appears irreducible. However, this misses the big picture of how evolution works and how functions often coalesce to form new ones by recombination, since this is generated in one or two steps, selective pressure all the way is still achieved. Now, this is true of many structures and functions, such as blood clotting (the whole chain is homologous and formed by serine duplication) or the flagellar motor (all homologous proteins, but comprised of the recombination not of individual proteins, but rather pre-existing structures, such as, in this case, the Type III secretor system of bacterial toxin pumping). The process of such exaptation effectively answers his idiotic point about the development of functions requiring interaction with the abiotic environment. The technical definition of speciation is a break-off where the break-off population may no longer exchange genetic material with its predecessor population. This almost always occurs when two populations of organisms become geographically separate, and therefore are subject to different evolutionary pressures and different gradients of morphological change. After all, animals in a pole environment have very different needs to those in a desert environment. The slightest and most subtle change in pressures can have far reaching consequences which is what makes evolutionary trajectories so complex. An interplay of factors will determine the shaping of the morphology of organisms, which include abiotic factors (food supply, weather patterns, geography) and biotic factors(predators in the area, disease vectors and predator/prey cycles).

Before delving into to inheritable trait and chemical encoding, we must understand this principle of the struggle for resources. Essentially, organisms struggle to survive. They fight. It is intrinsic to the nature of organisms that, being that they are the vehicle for a code whose sole purpose is self-proliferation, that they survive, which requires they gain the resources they need for survival and reproduction- food, water, shelter etc. Organisms are in competition with other organisms for resources and the variability inherent in the passing of inheritable DNA from parent to progeny means that some organisms may be better at the exploiting the environment for the gaining of resources than others, hence allowing more reproduction and the proliferation of this trait. Without this there can be no evolution. The precise molecular mechanisms by which this variability may generate the structures of complex life which allow the organisms to better exploit the environment does require some tertiary education in molecular biology to understand.

The points about deleterious mutations and DNA "choosing" are simply stunningly idiotic.

There is no “magic” or “unseen force” which guides evolution. We are not talking about Smith’s invisible hand. Rather, the fittest organisms will survive. Nature is not “selecting” anything. It is simply that if a trait is favourable, the organism will survive, replicate and the trait will be propagated, and vice-versa for deleterious mutations. It is truly that simple.

This is the crux of evolution. The process by which the favourable traits are selected and the deleterious ones removed. As such, it is forced in one and only one direction: towards the organisms being in better symbiosis with the environment. And there must be selective pressure all the way. Evolution is best described as raw, brute force which sieves favourable traits. However, there is no one doing the selecting. What “pushes” evolution is simply that organisms must survive by any means necessary, and the genetic code provides the traits by which they may better survive and reproduce. It is a struggle between biology and the environment, where biology is struggling for survival and nature is forcing an improvement in biological structure.

We must understand (and we will) that all life is based on the same chemical code of replication, and that the random variation in this code is forced to develop and accumulate into more advantageous sequences for the survival of the organism whose phenotype it expresses. This is called gene level selection. All life is based on just one code, which we are about to explore. This code is the interface which expresses the phenotype of the organism, as such it is the master key for any evolutionary change. From a single-celled foundation 3.8 billion years ago, the process of evolution has been the expansion of this code via homology, and the constant refinement in as many ways as possible . In this way, it is possible to look at the entire of biological life as a single, massive, set of genetic information struggling towards refinement and improvement such that the information expresses better ways for the organisms for which it is expressing to better survive in the environment. This raw force of the struggle for existence is what allows the generation of all the complex life we see around us, as a mutating continumm being expressed in the form of an ever-changing set of replicators buried within which is a drive for replication and hence the survival of the carriers (this was unknown until it was discovered by Richard Dawkins in 1976). Indeed, the refinement of the genetic code by means of the prorogation of the variation which the code exudes is surely a vastly more powerful technique for creating complex biological structure than is a loving creator assembling pieces of a flagella motor as though it were a jigsaw puzzle. The real reason that evolution, then is so appealing as a theory for the explanation of these structures (in addition to the ridiculously massive amount of evidence available for it a tiny chink of which was presented in my other essay) is that it is simply so powerful because there is simply such a vast number of organisms and such a vast amount of replication and hence such a vast and hyperbolically multiplying amount of variation, all being forced in the same direction by the struggle for existence. As Darwin realized, the process requires this vastness.

We must remember that evolution is all about selective pressure. It can fashion structures and functions just as well as any designer due to sheer brute force, but it is blind. It has no foresight, which means that there must be selective pressure at each increment of the generation of a new trait otherwise the trait cannot proliferate. Indeed, this is the basis of Behe’s “Irreducible complexity” argument regarding some structures which may render constant pressure impossible (ie the all or nothing dichotomy), but as we shall soon see, this is false.

The different methods by which genetic variation occurs:

As I promised, this part will be perhaps one of the most technical parts of the piece, so bear with me. The generation of new genetic material by which an advantegous trait may be gleaned is a complex process indeed. There are several ways in which it may be done:

Mutation mechanisms

All of the processes of variation in genetics occur via mutation, that is the random change in DNA as it is passed to progeny. Without these mutations, there can be no evolution. An extremely technical explanation of how this mutation may give rise to novel new protein combinations is given in this essay:

We shall start first by examining the mutations that occur in prokaryota (bacteria, since they are simpler to understand).

That essay outlines one of the major mutation mechanisms, indeed, the most critical mutation mechanism: Homologous duplication.

Homologous duplication occurs during failed cell division. A cell attempts meiosis or mitosis, and fails partway through the process, hence only a portion of the DNA is duplicated, and is retained seeing as a new cell has not been created. If this is the case, the cell in question has excess genetic baggage, and this genetic baggage may diverge from its role by means of the mutation mechanisms which are detailed below. Since it is superfluous, it can mutate solely on random frequency probability, and hence these mutations may create a new genetic function from a copy of the old one.

Homology is critical in evolution. As I explained in the proteomics essay, all of life is homologous, all of the genes and proteins of life have a quantifiable relationship with each other which indicates that they came from a common ancestor the divergent duplication of whose original genetic material has produced all of the diversity of life. Indeed, one of the greatest evidences for evolution is that this homologous relationship indicates precisely that life originated from a common ancestor. This was exactly the point I made in the proteomics essay.

Proteins, as I outlined in the essay, are the bulk of the structure of biological organisms, exempting water they make up 2/3 of any organism by mass. Hence, the creation of new proteins by means of duplication and divergence is a critical mechanism for creating novel organisms. The creation of new proteins underlies the creation of all new biological structures in organisms.

Homologous duplication may be regarded as the fundamental process which generates the raw material for which the next stages of refinement and divergence may take place.

Recombinative mutation: This mutation may cause pieces of DNA to realign or flip positions, it is caused by the mis-slotting of strings of DNA, as a result, a novel string has been produced. Now, I detailed this mechanism precisely in the other essay. Since the same domains in proteins crop up so often in ubiquitous proteins, recombination has been a critical function for the creation of novel new proteins for the creation of new phenotypes. The creation of new proteins from old ones is a critical mechanism in Eukaryotic evolution, since Eukaryotes more or less have the same proteins, with very little major divergence in the protein spectrum. The originalities, then, in the Eukaryotic proteome are produced by the rearrangement of pre-existing proteins.

Recombination and Homologus duplication are two of the most important mechanisms, because they indicate that the all the proteins and exons for all of life can be traced via homology back to primordial life, and the distance between the diverged proteins in terms of time can be measured in terms of how different they are from the original in terms of point mutation.

Now, these homologous mutations and recombination of the homologous copies are important for the generation of new proteins for phenotypic alteration, but the genome does much more than hold protein codes. A cell is much more than a protein factory. A cell must also decide when to manufacture proteins based on external and internal stimulus, and the rate of transcription and translation to determine how much protein is produced. In the case of multicellular organisms, it is exponentially more complex, since the genes must also decide where the proteins are manufactured. The latter is utterly critical to Eukaryotic evolution and is the key mechanism for the generation of complex biological structures such as the heart, the eye etc, since it is the basis of embryonic cell differentiation and positioning. This means that we cannot merely examine the effects of mutations which create and alter proteins, we must examine those of the regulatory DNA. Regulatory DNA is just that, it regulates. It codes for no proteins, rather it flanks the exons and controls their rate of transcription ,as well as where they are expressed in multicellular organisms, and when they are expressed based on internal and external stimuli. The result is a very complex Gene regulatory Node Pathway (GRNP), the alteration of which may produce new and innovative biological structures in multicellular Eukaryota, the precise mechanisms of which will be detailed later.

The genome is complex and intricate, but in Eukaryota, the way it is organized is just awful. It is in an alarming state of disarray. Exon chunks are strewn all over the place sandwiched between enormous and mostly useless strings of introns. What is the reason for this alarming lack of genetic housekeeping in Eukaryota? Simple, the common descent means that Eukaryota have not shed their excess baggage. They simply retain useless genetic information like a mass of old papers since it would take more energy to shed it than it would to simply retain it. Hence, Eukaryota simply retain much of their evolutionary "junk DNA" as dormant, nonexpressed strings of nucleotides which don't actually do anything, except, of course, help molecular biologists sort through evolutionary relationships. As evolution goes on, of course, this extra DNA just piles up, for there is no need for Eukaryota to shed it. This is clear indication of common descent of Eukaryota. Indeed, in humans, only 9% of our genome appears to have any function whatsoever, and thus far it has been confirmed that at least half of it is "safe for recombinative excision", which simply means that the deletion of it makes no change in the organism.

This contrasts prokaryota, which are small and energy efficient organisms for which small genomes are clearly advantageous. The result is that they have a much higher exon concentration and much less regulatory DNA (little regulatory DNA is required for a functional organism). The result is that they are much more genetically distinct and diverse than are Eukaryota.

Multicellular Eukaryota, being much bigger and much more complex than Prokaryota, are actually much less diverse. There are vastly more fundamental constraints and requisites on physiology, cell dynamics and anatomy in a multicellular organism than in a single-celled one. As a result, Prokaryota are vastly more diverse than multicellular Eukaryota, and are also much more diverse than Single-celled eukaryote (since Eukaryota are much more complex than prokaryota, and single-celled Eukaryota, in turn, are much more diverse than multicellular Eukaryota). This is evident if we examine the base-pair span relationship in different domains of life:

The majority of changes between multicellular organisms are quantitative for this reason. So, when creationists and ID proponents get starry eyed over the apparent phenotypic diversity over animals, and then dismiss solid bacterial evidence for evolution, they are displaying ignorance since multicellular organisms are vastly more rigidly similar in biochemistry than are any prokaryota. I share a higher percentage of DNA with the potted plant on my desk than do two prokaryotic species picked at random. It is for this reason that bacteria account for 99% of all species on Earth, and will always be the dominant arm of the biosphere as long as sustainable life exists on the planet. This is also why for the bulk of geological time, our ancestry were single celled organisms. So, again, I iterate that when the creationist despairs over the apparent vast differences between animals, but then dismissed observed bacterial speciative events, their ignorance rises to surface in the most amusing way. In terms of the biochemical spectrum, all multicellular Eukaryota are extremely closely related and that the generation of new species is so incremental and in terms of time slower than bacterial change is merely because bacteria reproduce exponentially faster.

For this reason, the utterly vast majority of mechanisms common to life were in place by the time the transition to multicellular Eukaryota was made after the rise of the Eukaryotes during the Oxygen Catastrophe. And it is for this reason that scrutinizing multicellular evolution so heavily while dismissing the evidence from the more easily observable bacterial evolution, is deeply dishonest for creationists. Granted, we can observe animal evolution very well, and our molecular techniques allow us to read it just as well as we would bacterial evolution, however, we must remember that we share far more in common with say, tucans, than the average soil bacteria shares with the average bog bacteria, and when examining the phenotype diversity of animals, we tend to forget this.

In another essay, we will be examining the exact mechanisms of how Eukaryotic regulatory DNA creates complex biomolecular structures, they have to do with frightening phrases such as Hox genes, heterochromatin, the position vateriegation effect etc. Hox genes explain why multicellular organisms arose so fast (The Cambrian explosion) and why animal evolution happens much faster than bacterial (in terms of generations, NOT years) and how phenotypic diversity and complex multicellular structures form and develop. This, in essence is evolutionary developmental biology, the synthesis of embryology with evolution. It is a radical new field which overturns old thinking. Namely, instead of a vast number of tiny incremental changes driving animal evolution, more significant Hox gene tweaks allow for the development of new structures in utero. This helps to overturn many creationist arguments, including irreducible complexity. However, it is not the topic of this essay. For now, we must press on.

Prokaryotes have the ability to directly exchange DNA via the uptake of small fragment of DNA of other members of the species which are encapsulated in tiny viral packages called plasmids, which are circular rings of DNA, which may be taken in by other prokaryota, hence allowing the rapid sharing of information between bacteria, which may a factor in bacteria gaining resistance to drugs so fast. It is very difficult to track the relationship between the fragments for obvious reasons, and this form of genetic exchange is called horizontal transfer, which is simply the transfer between two organisms of any information which is not from parent to progeny. In this case the fragments are called xenologs.

Hence we arrive at a critical concept: Vertical and horizontal transfer. Vertical transfer is merely the transfer of material from parent to progeny, and the result innovation that occurs from the recombination. This is due to the creation of alleles by paired sexual reproduction, whereby the two genetic characteristics are different and the progeny will inherit different characteristics from their two parents. Allele frequency is a critical concept in evolution since it determines the concentration of variations in sexually reproducing organisms.

 This poor moron (who probably wonders why that big orange thing in the sky rises every morning) also has no idea how DNA/Protein/RNA works, and makes an idiotic, cacaphonic strawman of abiogenesis and chemical evolution, which does not say that a random "glob of protein" (does this fuck even know what proteomics is?) just "appeared" while interspersing similiar phrases attempting to reduce it to the level of his childish idiocy (such as "sludge" and "glob of goop&quot. Abiogenesis is so poorly understood by so many idiots such as this. Also, he really has no idea of the DNA/RNA/Protein relationship. Allow me to explain:

I suppose that before beginning to explain why, an explanation of fundamental concepts is in order. To understand evolutionary mechanisms, we need a very deep understanding of genes and proteins. Since an advanced expalantion of evolutionary genetics is covered in an essay I am writing called Hox Flow Mechanisms and Their Effect on Evolutionary Phenotypes and Structures the bulk of this essay will be about proteins. Why genes and proteins? The relationship between genes and proteins, and their interactions with RNA is deep and ancient. Many times have I said that only someone who truly understands the interlocking three pillars of molecular biology with the depth that comes with years of study is the only person who has any right to comment on the validity of the theory that life evolves.

Essentially, a protein is a string of amino acids, usually 500-2000 amino acids long. The whole of life depends on proteins. Everything else, save the genes, is a mere passive bystanders in a biological dance of life. When we observe the cell, we are in essence observing proteins. Proteins control movement (motor proteins), the control structure (structural proteins), they control concentration (transmembrane proteins), they control ion gradients (pump proteins), and most importantly, they control every single chemical reaction in the body (enzymes). Proteins don't just control the body, they are the body. All proteins fold up tightly into one highly preferred conformation. There is no limit to the number of tasks they do in the cell. Proteins can be subdivided into two large classes, the globular proteins fold up into irregular ball-like shapes and fibrous proteins. Nearly all globular proteins are allosteric, which means they can adopt two slightly different conformations, this means they have two binding sites, one of which is for a regulatory molecule, and the other is for the substrate. Allosteric control is very complex. Suffice it to say for now that it works on either negative or positive feedback (ie the regulatory molecule increases the protein's affinity for the substrate, and the other way around, or the opposite, the regulatory molecule decreases protein affinity for the substrate, which of course, would be reciprocal. In this way, regulatory molecules can turn the protein on or off, and in negative control, there is a tug of war between the regulatory ligand and substrate which are reciprocally affected by each others concentration in the cell.

A short summary of biological proteins would look like this:

A protein is a specific type of biological polymer made up a specific family of chemical subunits called amino acids. There are 20 biological amino acids, and they are distinguished by the fact that they all have a central alpha carbon, which is attached to an amine group (-NH2), a Carboxyl group (-COOH), a hydrogen, and a side chain. It is the side chain that gives each amino acid its properties, and each of the 20 has a different side chain. Proteins can be anything in length. Usually it is 50-2000 amino acids long, and the longest ones can 7000 amino acids long. The interaction between the side chains (which is determined by charge, since three are basic, four are acidic, nine are nonpolar and five are polar but uncharged) determines the shape of the protein. For instance, the nonpolar side chains are all hydrophobic (water hating) which means the protein will fold up in a manner where the nonpolar side chains are facing inwards and not exposed to water (this is the most energetically favorable conformation). This is just one of many different subtle interplays between amino acids that determine a proteins shape. However, nearly all proteins fold spontaneously in a solution, indicating that all the information necessary to fold it is stored in the amino acids.

Proteins are:

Structural: All large structures in the body are almost certainly composed of structural proteins. Adding repeated protein subunits allows for geometric assembly of thousands of structures. For example tubulin can, by readdition of the tubulin subunit, assemble the microtubules of the cell. Actin is a fibrous, ropelike protein that can assemble into fibrils, like most fibrous proteins, which is a long sheet of fibers arrayed together. Actin is the fiber responsible for muscle contraction, another example is elastin, which is made of a loosely bound collection of elastin polypeptide chains, which, when bonded to each other, make a rubber like sheet that gives skin its property of stretching without tearing. Many structural proteins can self-assemble just by the repeated addition of a single protein. For example, the capsid, which is the coat of a virus, is a spherical structure which is made by no more than 60 identical proteins added together to make a perfect sphere.

Enzymatic: Globular proteins function as enzymes, which speed up all the body's chemical reactions. Enzymes are better catalysts than anything man has, and can speed up a reaction by a factor of 100,000,000,000,000 (100 trillion). They control the rate of the thousands of reactions in the cell, and by regulation and coordination and feedback loops, create massive, intricate metabolic pathways. All enzymes have an active site, which the molecule to be catalyzed (any molecule that binds to a protein is called a ligand) attaches to for catalyzation of whatever reaction is needed. Usually enzymes operate in steps, so the product of one enzyme becomes the target for the next, in this case, the molecule is called a substrate.

Transmembrane: Proteins can be arrayed across the membrane of the cell and control the concentration of various chemicals inside, allowing certain chemicals in and out. They are usually powered by ATP hydrolysis and usually control the flow of small ions like calcium and potassium. Trasmembrane proteins are technically a class of motor proteins, which are detailed below. Transmembrane proteins are important in cell regulation and enzyme kinetics. In muscles they are particularly important as it is the flow of Calcium ions out that powers the muscle contraction. They are very important in neurons and synaptic vescicles as the flow of ions (calcium, potassium and chloride) is what creates the energy gradient which holds the information the neuron is carrying.

Motor proteins: All proteins have precisely engineered moving parts, but motor proteins especially so, since a tiny movement has to induce a major conformational change. For instance, the protein myosin has to control muscle contraction, which, as you can imagine, is a tremendous organizational problem. Many motor proteins have the very impressive ability to “walk” across structures like microtubules and DNA polymers. This is an autocatalytic inbuilt function of the protein. It results from the protein having three distinct conformations, and the protein switches between them via ATP hydrolysis. Since ATP hydrolysis is extremely energetically favorable, the protein is forced to move in one direction, since ADP condensation is almost certainly not going to occur. The protein is forced forward by a catalyst called Adenine nucleotide exchange factor, which releases the ADP after hydrolysis causing an ATP to bind to the regulatory site almost immediately. In this way the protein is forced from conformation 1 to conformation 2 to conformation 3 and then back to conformation 1 and so on.

This cell’s wall will be studded with transmembrane proteins which control things coming in and out of the cell (organic molecules in, waste gas out). Meanwhile, inside the cell, enzymes will be running the day-to-day operations of the cell. Structures inside the cell (usually made of proteins) needed to maintain it will be being broken down, assembled, and repaired in a series of complex pathways all controlled by enzymes. Meanwhile, the cell needs energy and raw materials, so it imports organic molecules (aka “food) and breaks it down into simple subunits (this process is controlled by enzymes) which are then used for energy (a process which is also controlled by enzymes) or used to construct large cellular structures (this is also controlled by enzymes). For all this to happen requires a lot of chemical messages to fly between lots of different parts of the cell so that the cooperative process keeps going, and all different cellular projects are in communication and taking cues from the environment for what to do (these processes are controlled by signal integrating proteins, signal amplifying proteins and signal transducing proteins).

Controlling all this is the genetic code. The genetic code holds the “master key” to all the proteins. The rate at which proteins are assembled from genes is controlled by other genes, which in turn usually end up being controlled by other genes. Since proteins work in teams, the concentration of each different protein, as controlled by the genetic code, affects the cell as a whole. Most of the time, the demand for various products operates on a feedback loop. If a product is needed, it triggers a stimulus which sends a message to the genetic template. This can result in a particular gene being switched on or off or increasing rate of production or decreasing or a host of other things.

In other words, the genetic code of a cell functions like a microprocessor. It takes input from the environment, processes it, and delivers an output. In this way, the whole balance of the cell can be controlled by the genes. However, this analogy is not entirely accurate since the relation between proteins and genes are reciprocal ie proteins can control genes (these are called DNA binding proteins).

Now, onto protein generation. 

This (protein assemblage) too, is not chance. The simpleton would 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.

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. 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? After all, we now understand due to the RNA world hypothesis the bulk of the processes behind the formation of proto-biological pathways like glycolysis and photosynthesis, and that the nucleotide handle on nearly all of the carriers (like Uridine Diphosphate Glucose and Acetyl CoA are due to the electrolytical interaction with RNA proto-biological structures, especially for UDP)

Lastly, Common Descent is also heavily corroborated by ERV tracking and the vertical transfers in Mitochondrial DNA, which is often overlooked by geneticists because it is not very interesting, but I noticed it because it is such an excellent indicator of common descent.

Endogenous retroviral insertion occurs when a retrovirus reverse transcribes it's own RNA into a host's DNA by means of polymerase RNA-DNA conversion, 3' and 5' enzymatic degradation and intergrase fusion. Retroviruses are the only organisms that can do this. That is what makes HIV so deadly. The ERV insertions are rare and very random. Although complementation ensures they can only bind to specific points on the host's genome, the amount of possible insertions that the ERV could transcribe, not to mention the fact that this has to be to the power of seven to account for all seven retroviruses, and of course, the fact that it is a very rare occurrence and the fact that even a single transcribed piece has numerous choices of insertion due to multiple duplication errors that exist in Eukaryotic genomes means the odds of finding even just one insertion (let alone 8% of the genome for humans alone) on one identical position in the chromosomal karyotype would be astronomical. And then, that number has to be raised to the power of seven, then multiplied by several thousand to account for all the possible transcribable genes, which has to multiplied by 10 again to account for the duplicative errors, and that doesn't even factor in how rare the insertions are.

The only way it is possible that we can find large strings of ERV's on identical interspersals throughout the genome of species throughout every eon is because of common descent.

It is empirically demonstratable that mitochondria are the result of billion year old symbiosis between ancient oxyphobic bacteria and proto-eukaryotes. This is the reason they have their own little genome. The mtDNA genome in humans is only 16,000 base pairs. Prokaryotes have a remarkable ability to exchange genetic material by a different process which is critical to bacterial evolution. This is called horizontal transfer. Vertical transfer is an ability eukaryotes do not have because their DNA is enclosed in an intercellular packaged membrane (hence the name eukaroyote). Vertical transfer occurs when bacteria simply exchange genes by passing them through the cell membrane to each other. This can occur either by direct junction fusing or literally uptaking of the new material. Prokaryotes can take any peice of nucleic acid string and simply incorporate it immediately because their DNA is not kept in an intercellular membrane.

So, mitochondria, as ancient prokaryotes, of course keep their DNA is a loop strand like every other bacteria. Indeed, mtDNA also undergoes transfer. This is very rare and obviously useless. In this case, it is intracellular thus the transfer is into the nucleus of the host cell, where the master genome is stored. Such is termed mtDNA migration.

I think mtDNA migration is even better than ERV because the probability is even lower by several orders of magnitude that we could find mtDNA on identical positions of the genotypes of multipe species throughout multiple eons without common descent whereby the offspring would inherit the mtDNA. The best part is that obviously, as time passes, the amount of mtDNA in the master genomes should accumulate, since more horizontal transfer is taking place over longer periods of time, and this should still turn up on the same positions in the genotype. What a surprise! It does.

Without common descent, the probability of individual horizontal transfers accounting for entire species inheriting identical mtDNA which remains so throughout geological eons and continues to accumulate and end up in the same places is so low the number is unfathomable.

Also, a false dichotomy is made in the implicit language

Let us begin with something simple pertaining to false dichotomy fallacy. Many theists argue, fallaciously, for the existence of God based on the idea that existence is too complex and intricate to have formed randomly, and often attempt to make a fallacy of conflation between “not God” and “randomness.

The bifurcation occurs because the argument rests on the false dichotomy that “if not God, then chance”. This is fallacious because there is a third alternative (hence, we have a triconditional premise, which means that bifurcation is fallacious). That third alternative is natural process, which is not random, which is guided by the laws of physics and chemistry and such, but has no conscious will behind it. The bifurcation occurs because the theist makes the unjustified assertion that conscious will (ie a “mind” such as “the mind of God”) is necessary to create the order we see around us because it cannot be random. While it is true it cannot be random, this does not necessarily imply that it must have conscious guidance, because that fallaciously implies that we have a dichotomy between “conscious will” and “randomness”. In reality, we have unconscious, but certainly not random, processes which form the order we see. The process of biological evolution, for example, is blind-guided. But it is most certainly the absolute and precise opposite of randomness. This is true of vast numbers of natural processes which explain why things are the way they are, from star formation and cycles to geological columns . Everything down to the quantum level and up to the macrocosmic scale is governed by sets of physical and chemical laws which have no consciousness behind them, but still produce complex Order. In reality, the natural processes which do produce the order we see around us are extremely complex and anything but random. They are much, much more capable of producing natural order and complexity than we are at producing artificial complexity.

I admit, this one is quite instinctual. Since we are conscious entities, we tend to have some confirmation bias on the necessity of consciousness for anything to occur which is not random. In reality, this is not the case (and it just begs the question anyway). The problem is that we are used to the notion that only conscious entities may produce complexities, because that is what we do (this is why the unusually dim may compare natural structures and order to our artificially generated devices such as watches as per Paley). Hence, we tend to fallaciously conflate “not conscious” with “random”. This is a bifurcation which is false.

Many theists hence make the following statements

“Evolution is just randomness”

“abiogenesis (actually, most of them, fallaciously, say “evolution”) says that a bunch of molecules randomly collided to make life

Or more usually “evolution (again, fallacy of conflation) says that life came from rocks” (Take note, Hovind, this is factually false as well as fallacious)

“The Big Bang was just an explosion which was purely random”

And then use these falsehoods (which are based on the false dichotomization of “randomness” and “God” to make the following a posteriori statements:

“Life could not have formed randomly. Therefore God”

“Life appears designed. Therefore God” (This does not mean anything since “appears designed” is merely

Which are all false since they all depend on the false dichotomy.

What a fucking idiot. My brain is bleeding. I think everyone in the room just got dumber.

DG you are like a nuclear bomb on theists. I think I'll just stand out of the way.

I am no biologist by any stretch. But it is idotic to ignor the simplicity of an atom. The mistake apologists make is assuming complexity from the start. An atom is not complex. The bonds between atoms are simple positive and negitive relationships.

Considering the infinate atoms, not only on this planet, but in the universe, it does not sprize me one bit that complex life comes from something as simple as an atom.

This is nothing more than willfull ignorance in an attempt to justify hocus pocus in the end.

However, when you stick a magical sky daddy into the mix, it makes no sense at all. You cannot cherri pick science. If the theist is going to accept that atoms exist, and at the same time sell us the crappy idea that daddy can manipulate googles of atoms all at the same time to creat Adam out of dirt, is nothing more than a piss poor atempt to justify alchemy.

What the theist cannot demonstrate is HOW such a claimed being could do this. There is no way to falsify such a claim. "God did it" is a claim, not an explination. "Thor did it" would be as aceptable if claims always passed as an explination.

Somehow the sky daddy POOF, magically makes dirt instantainously turn into an adult male? Ok, and this is just as demonstrable as being able to get laid in an afterlife by 72 virgins.

 The simplicity of an atom is a valid, demonstrable and falsifiable fact of science which doesnt need ancient fairy tales to prop it up.

This is just another attack on science because the theist doesnt want to admit that fiction is fiction. 

The guy flys off the rails in the very first line. "There's no way a molecular machine could develop out of nowhere..." Right there he betrays his ignorance of the subject matter and proves that he is either a) deliberately and dishonestly misrepresenting the evolutionist position or b) cutting and pasting from a creationist site without understanding what he's posting.

Not worth bothering with. Tell him to go read a book and when he understands why his first line is wrong to come back and try again.