Evolution 101 Gradual Evolution

As creationist screeds go, this is among the best I have read. Unfortunately, that only puts it among the best of a bad lot. Since you seem to have a sincere interest, I will respond in-depth. I will try to make this as understandable to a general audience as I can, but some of it will undoubtedly be a bit technical. You can either skim any parts that are too technical or ask questions and I will elaborate the best I can. I apologize for the length in advance.

Much has been debated in the scientific world and without as well about the origin of species, or evolution. However, people on both the proposing and opposing side of the issue really do not know exactly what evolution is. This sad fact has resulted in endless debates between people so fully entrenched in their beliefs that such debate is really just fancy arguing. Therefore, here is my endeavour at a balanced post about the pros and cons of gradual evolution. Just a note that this is trying to put extremely complicated theories into simple terms, but it would definitely help if a person had a basic knowledge of genetics, specifically in the area of mutations, to understand much of what is about to be said.

Gradual evolution, also known as Neo-Darwinism, is most basically the belief that everything we see is a result of billions of years of change. The belief originates with Charles Darwin, as the name implies. Darwin first got his idea for his book when he was told by the British governor of the Galapagos Islands that he could identify which island a tortoise came from by the pattern on the shell, as well as the shape of the shell and length of the tortoise's neck. Darwin decided to stay around to observe the other wildlife and discovered the now famous finches and their various differences. He decided to catalogue these differences and found that not only were they different in looks, but the differences had functional uses. Inspired by this, and a great number of other things, he wrote his book "The Origin of Species."

From this book, scientists have based many experiments and research hours probing the possibilities then opened up to them. The current theory, with the unveiling of the shape of DNA, has flowered fully.

I only have a few nitpicks concerning your introduction which was overall OK.

(1) The debates within the SCIENTIFIC world concerning evolutionary theory has been limited to peripheral aspects of the theory (at least since the 1930’s). The peripheral aspects include the importance of certain mechanisms other than natural selection, such as neutral selection, macromutations, the role of punctuated equilibrium, etc. There has been NO debate as to whether or not evolution has taken place. The evidence for that is so overwhelming amongst scientists that is considered a settled issue … it has.

The debate that has taken place over whether or not evolution is a real phenomenon has taken place in the political realm by people pushing a religious agenda.

(2) You have not written a “a balanced post about the pros and cons of gradual evolution”. You barely mention the TONS of evidence that support it. For instance, you make no mention of the nested hierarchies we see in taxonomy. You make no mention of the fact that there are no out-of-place fossils. You make no mention of the data on comparative anatomy that suggests common ancestry across virtually all taxons. Instead you quibble with antibiotic resistance in bacteria and sickle-cell anemia. Furthermore, you ignore the scientific response to the quibbles that you mention.

That’s OK. If you were going to write a “balanced post” then it would have to be book length with almost no mention of the different forms of creationism (since it is irrelevant to the evidence). I would not expect that here. But you should be upfront about it. You are writing a creationist screed. It is your contention that evolutionary theory is not as secure as scientists say it is. You believe that creationism explains some things better than evolutionary theory does. Fine, go ahead and present your evidence that it is so. Just don’t try to give the impression of impartial objectivity when it is not there.

(3) Your term “gradual evolution” would be more properly be referred to by its technical name, PHYLETIC GRADUALISM. That means that speciation caused divergence at a rather regular slow pace. Neo-Darwinian evolution has not been wedded to phyletic gradualism since the publication of GG Simpson’s book, TEMPO AND MODE OF EVOLUTION.

(4) Darwin came to his idea of evolution by means of natural selection by a long line of reasoning. He certainly did NOT have an epiphany when the governor of Galapagos told him about being able to identify the island of origin of the turtles. If he had he would have been more careful as to labeling of his specimens. He failed to record the islands that he took them from, MUCH to his later regret. Fortunately, others on the expedition also took specimens and they DID record which islands they came from. Darwin was able to crib notes from them on the islands of origin of not only the turtles but mockingbirds and finches among others.

What a lot of people don’t realize is how much thought Darwin put into his theory. He returned from the voyage on the Beagle in 1836. It wasn’t until two years later in 1838 that he opened his first notebook on the “transmutation of species”. He began to write what he called his “big book” on the subject in 1844. In 1858 he got the paper from Alfred Russell Wallace that made him think he better publish soon or have his idea scooped. ORIGIN (which Darwin referred to as a abstract of his “big book”) was published in 1859, 23 years AFTER the voyage on the Beagle ended.

As such it is impossible to set a single instance as being the moment when it all came together. Darwin himself, credited reading Thomas Malthus for his “eureka” moment; but in his notebook on evolution he barely makes mention of his having read it. I tend to think that it came about gradually.

The two main engine parts in evolution are mutations and natural selection. Mutation is the first domino to fall in the chain of dominos. A mutation is defined, simply, as a mistake in the copying of genetic information (DNA), resulting in a possible change in the type of protein coded for in a given gene. Mutations occur at a slow rate (Out of the 30000 possible genes in the human DNA strand, only two mutations are believed to occur) and are generally unnoticed in the organism itself. However, there are mutations that do not go unnoticed, These fall into three categories, Nonsense mutation, addition mutations, and subtraction mutations.

Nonsense mutations are mutations where a replacement of a base pair causes the gene to call for a stop in the transcription process. This can, and usually does, truncate the protein the gene originally made and causes the process of that gene to deteriorate or change completely.

Addition and subtraction (deletion) mutations are where a base pair is added or removed from the gene, causing a flood of missense and nonsense mutations to follow. This also completely changes the gene.

This is the first part of the process and the credited source of new genetic information in the theory.

Again this is mostly OK. My comments here are like those above, mostly minor quibbles.

(1) By using the metaphor of dominoes falling you give the impression that mutation and natural selection are step-like cause-and-effect processes. First a mutation occurs and that causes natural selection to either keep it or eliminate it. This is somewhat misleading.

Mutations occur all the time. Natural selection is working all the time. A mutation that may have occurred in an ancestral species could have been passively passed on through several descendant species without any selection taking place. Millions (perhaps even billions) of years may pass before an organism finds itself in an environment in which that mutation makes a difference to its reproductive success. It would only be at that moment that natural selection would kick in.

As a general rule it is not the mutation that causes natural selection to act on an allele, it is an environmental change that does so. This remark will become important when I discuss your section on natural selection below.

(2) You say, “A mutation is defined, simply, as a mistake in the copying of genetic information (DNA), resulting in a possible change in the type of protein coded for in a given gene.” A more useful definition of mutation would be simply to say, “a mutation is a mistake in copying the DNA sequence”. Your definition creates problems when we look closely at the genome.

For instance, most eukaryotic genes are segmented. There are stretches of DNA whose code will ultimately lead to the expression of specific amino acids in proteins. These are called EXPRESSED SEQUENCES or EXONS. However, between these exons are sequences that get processed out of the RNA and do not ever get expressed into proteins. These are called INTERVENING SEQUENCES or INTRONS. Does an intron constitute genetic information? Or is it trash with no informational content? Or perhaps play an important role in differential expression of genes? A mutation that occurs in an intron will not have an effect on the type of protein coded for, but it may have an effect on the expression of that protein. For instance, the protein my not be produced in as much abundance as normal.

Also only about 1% of the human genome encodes for protein. If there is a mistake in copying the genetic code there a mutation? It is very unlikely to have any effect on the fitness of the organism.

Finally, some of the DNA codes for RNA sequences NOT proteins. A mistake in copying that COULD have profound effects on the organism’s fitness.

Under my definition there is no question, a change anywhere in the genome is a mutation. For the purposes of my response for the rest of this section I will be using MY definition of a mutation.

(3) The cells of the body can be roughly divided into two groups; somatic cells that make up the organism’s organs, and sex cells that will differentiate into gametes (eggs and sperm). If a mutation occurs in a somatic cell it will have no effect on succeeding generations. Thus, mutations are of importance to evolutionary theory only insofar as they occur in sex cells … and even then only in sex cells that develop into new organisms.

It has been a while since I checked the literature on mutation rate and the following discussion will be from memory. I am confident of the principles behind the discussion, however, the details may have changed since I last looked.

The human genome has about 3 billion base pairs. The spontaneous mutation rate is about 1 per million base pairs copied. That means that in a typical cell division there are about 3000 mutations. However, we are eukaryotic organisms and we have enzymes that specifically try to sense and repair genetic damage. They repair about 9 out of 10 of the mutations. That leaves about 300 mutations per cell division. These occur randomly over the genome. But only about 1% of the genome codes for genes. Therefore we average about 3 mutations per genome.

Mutations can occur by a number of ways:

Point mutations – These are changes in which a single nucleotide is (a) miscopied to another nucleotide, (b) inserted into the sequence, or (c) deleted from the sequence.

Line inserts/Line deletions – These are mutations in which a number of nucleotides are inserted/deleted from the sequence.

Inversions – This type of mutation occurs when a segment of DNA gets clipped and spliced back on in the opposite direction from which it originally was.

Translocations – This happens when a piece of one chromosome gets clipped off and then spliced back on to another chromosome.

Segregation distortions – This happens during anaphase of cell division. Instead of chromosomes going to opposite poles as they should, occasionally some go to the same pole as their paired chromosome. This can lead to large increase/decrease in the amount of DNA in an organism’s genome.

Mutations that affect gene expression – I have already alluded to one type above … a mutation that causes a gene not be expressed as abundantly as it did before.

These types of mutations can affect the host organism in a number of ways. For instance, point mutations involving the miscopying of one nucleotide for another is likely to be have no observable effect. A point mutation involving an insertion or deletion, on the other hand, creates a frame shift. The amino acid sequence of proteins is determined by the sequence of DNA nucleotides taken 3 at a time. Inserting or removing one nucleotide shifts the frame and can change all downstream amino acids. This might seem like a devastating mutation, and it can be. However, it usually isn’t. If may occur in gene that makes no difference to the organism’s survival in the environment it finds itself. Or even more likely, since we have two copies of genes, one from our mother and another from our father, even though one copy is devastated the other functions well enough so that even a frameshift mutation does not affect the organism’s fitness.

Most offspring are about equally fit as their parents. That is they produce about as many viable offspring as their parents did. Therefore most of these mutations, even the ones affecting the gene-encoding regions of the genome must be neutral mutations. So contrary to the popular notion that most mutations are harmful, they are actually neutral, neither benefiting nor adversely affecting the host organism.

After mutation, natural selection takes over. The title given it is misleading in name, since natural selection isn't intelligent, and therefore is not capable of choosing or selecting. It is but a passive process that causes the weaker organisms that can't bear as many offspring to die off and the stronger organisms to flourish. It is at this point that mutations are revealed as beneficial or deleterious.

It is these two processes that lend credibility to the theory. Mutation providing new genetic information at a slow but steady rate, and natural selection reinforcing the beneficial mutations while weeding out the weak mutations.

This discussion of natural selection is pretty weak.

(1) Natural selection is working all the time. Strictly speaking it doesn’t even require mutations. An organism can have an acquired injury that makes it more subject to predation. That organism is likely to be selected against even though there is no gene for his defect. Of course, such selection has no effect on the course of evolution. Evolutionary significant selection occurs only with traits in which (a) are inherited, and (b) for which have some variation within the organism’s gene pool.

Furthermore, there exist some special cases in which natural selection works in very significant ways yet no mutation is involved. Two of the most significant evolutionary events in the history of life fall into that category. All eukaryotic cells have mitochondria which are capable of producing biologically useable chemical energy from O₂, and plants have chloroplasts which are capable of fixing energy directly from sunlight into the chemical bonds of carbohydrate molecules. Both of these subcellular organelles apparently arose NOT through mutation, but by a process called symbiosis. Both had ancestors that were apparently free-living bacteria-like organisms. At some point another bacteria-like organism engulfed one and instead of ingesting it allowed the mitochondrion/chloroplast precursor to live within it to the mutual benefit of both.

(2) There is nothing wrong with the term “Natural selection”. It means just what it says … nature selects. The term selection does not necessarily imply intelligence. A lot of selection occurs without intelligent involvement. For instance, eggs are sized by having a conveyor belt bring them across platforms that sense their weight. If the egg is of a certain weight the platform lowers and the egg is put into a bin with other eggs of similar weight. If it weighs less than that platform specifies the egg is transferred to the next platform that responds to less weight. Eventually the egg will be with other eggs of its size. This is selection but there is no intelligent agency doing the selecting.

(3) Since organisms are complex, natural selection can be complex as well. Perhaps, it even qualifies to be a directly creative force in some special cases. I will give you a taste of one such controversial area in modern evolutionary theory, the evolution of evolvability.

As I said above we have enzymes that are responsible for sensing and repairing mutations. Ours works at about a 90% efficiency. However, some organisms have enzymes that do a bit better than ours and some have enzymes that do significantly worse.

Some organisms have evolved in environments that do no seem to change hardly at all. Others evolved in environments that fluctuate wildly. It turns out that those in very long-term stable environments have VERY efficient repair enzymes, those in constantly fluctuating environments have POORLY efficient repair enzymes. Why is that?

The idea behind evolvability is that organisms with very efficient repair enzymes are fitter in very stable environments, but organisms in which mutations (an hence variation needed for evolution to occur) build up faster are more fit in wildly fluctuating environments. In the wildly fluctuating environments, such an organism is more likely to develop a mutation that will allow its offspring to adapt. Thus, natural selection would favor an organism more likely to develop a mutation.

However praised the theory of Neo-Darwinism is, it is not without it's own stumbling blocks. First among these is that while mutations are rare, beneficial mutations are as rare as Quasars in the stars. As a matter of fact, the vast majority of mutations in DNA are either silent or deleterious. There are some exceptions that evolutionists have brought up, and I will deal with those.

First a couple of other quibble. Quasars are not all that rare. They are just very far away and are thought to be a product of the early universe.

Second, you are being misleading. It is wrong to classify mutations as beneficial, neutral, or deleterious without making reference to the environment they are in. NO mutation is going to be universally beneficial no matter what environment it happens to be in. Some mutations can be deleterious in one environment and beneficial in another. The most common case is for a mutation to be neutral for a long period of time, until a change in the environment occurs. At that time the formerly neutral mutation can have either a beneficial or a deleterious effect.

Since most organisms are well adapted to their local environments already, any novel mutation is of course most likely to seem to be deleterious. Suppose that such a mutation causes the organism to have a harder time competing with other members of its species. This may cause the organism to migrate, it may migrate to an area with a different local environment where the mutation will not be a problem or can even be a benefit.

First among these examples are bacteria and their ability to become immune to antibacterial agents. However, this is pointed out by Gould (More on him in the next blog) as what could be called an evolutionary cripple. Such an immunity comes from the loss of the receptor the antibacterial binds with. When returned to the control group (a group that was not exposed to the antibacterial), a couple dozen generations showed that the amount of bacteria without the receptor was decreasing while the control group was increasing. This shows that the mutation was not beneficial to the organism except in a rare instance.

You seem to be implying that antibiotic resistance in bacteria is always due to the loss of some gene product. That is not the case. Most antibiotics do not have a receptor on the surface of bacteria. The way antibiotics work is that they attack something vital in a bacterium but do not adversely affect us.

For instance the pennicillins attack bacterial cell walls. Our cells do not have a cell wall to attack. The aminoglycosides attack bacterial ribosomes which are different in structure from eukaryotic ribosomes (but are very similar to ribosomes found in mitochondria and chloroplasts). The fluoroquinolones attack an enzyme that untwists bacterial DNA. This enzyme is not found in eukaryotes.

Resistance to all of these antibiotics can be demonstrated in experiments. Take any bacteria you want and any antibiotic you want. Plate the bacteria on agar plates and it will form colonies. Each colony is a population of bacteria that are descended from a single bacterium. Therefore at one time there was a single DNA sequence. Any new trait must have arisen by mutation.

From that initial plating chose a colony of bacteria. It doesn’t matter which one. What you need to do is plate some bacteria on more agar plates except this time the agar is made up with different concentrations of whatever antibiotic you chose. You need plates in which the concentration of antibiotic is so low virtually all colonies survive, to plates in which the concentration of antibiotic is so high virtually all colonies are killed. Plot the number of colonies that survive as a function of the concentration of antibiotic in the agar plate. From this you can estimate the concentration needed to kill ½ the colonies. This is the LD50 (lethal dose 50%).

Next make up a mess of agar plates with an LD50 concentration. Plate the original bacteria on one plate. On the next plate, use bacteria from a surviving colony from the previous plate. Continue this procedure throughout. At the end recalculate the LD50. You are virtually guaranteed to see that the LD50 has significantly increased. In other words it will take much more of the antibiotic to kill half the colonies. You might even find that the antibiotic no longer has any effect on the bactria.

Now if you happen to also have expertise in molecular biology you can compare these bacteria to bacteria taken from the original colony to see what is changed. Here there is no guarantee on your results. Antibiotic resistance can be achieved in a number of ways and there is no predicting beforehand how whatever bacteria you chose will end up doing it.

I suspect your particular example derives from penicillin resistance. Penicillin attacks bacterial cell walls. It binds to a particular sugar-like molecule on the cell wall. SOME strains of penicillin resistant bacteria no longer make that particular sugar molecule. They achieve their resistance by not having a penicillin binding site. But there are other strains of bacteria that achieve penicillin resistance in different ways. For instance some pump out a chemical that breaks down penicillin’s biochemical structure. Others take up penicillin before it has a chance to do damage to the cell wall. These other ways do not necessarily involve a loss of anything.

The next example evolutionists have given in the past is the sickle cell gene, for while a person with the full gene (A homozygous S/S gene) would most certainly die, a person who only carried the gene (A heterozygous S/s gene) would experience a sort of immunity to malaria and certain other diseases. However, outside of areas where malaria is prevalent, this person has the possibility of giving birth to children with the homozygous gene. This makes this example hilarious every time I hear it, because we all know that the homozygous sickle cell gene will never overcome the homozygous standard cell gene.

You have a severe misunderstanding of what this example actually shows. It shows how natural selection works and how it differs from Intelligent Design. Natural selection has absolutely NO foresight. It cannot anticipate problems. All it knows is what provides a selective advantage with respect to a specific environment at the moment.

Sickle-cell trait, the heterozygous condition, offers a selective advantage to people in an environment rife with malaria. Malaria is caused by Plasmodium bacteria, (usually P. vivax or P. falciparum). These bacteria are transferred to humans during a bite from a mosquito. They form trypanosomes inside red blood cells (RBCs). Infected RBCs do not respire like a normal cell and therefore, tend to become acidic. RBCs with a single copy of Hb_s gene (the sickle cell trait) will form sickle-shaped cells in an acidic environment. These cells do not go through capillaries well so they rupture, releasing the trypanosomes into the blood stream where the body’s defenses can attack them. This effectively makes the person immune to malaria.

Unfortunately, a person with two copies of the sickle cell gene (ie a person who is homozygous Hb_s) will form sickle-shaped cells with no provacation. This leads to a lot of cells being ruptured, severely compromising oxygen transport and stressing out the liver. It will ultimately lead to the death of that person.

So on the one hand, Hb_s gives one a selective advantage if one has a single copy, but on the other hand it gives one a selective disadvantage if one has two copies of the gene. That means that IF a particular population is subjected strongly to malaria and the gene has not yet entered into the population, ANYBODY who may develop this mutation will be selectively advantaged. So will all this person’s offspring. And unless they have children with their siblings so will THEIR offspring. So long as the frequency of the Hb_s in the population is very small then almost anyone having it is likely to benefit from it. BUT as the frequency rises the likelihood of being homozygous rises. So at what level does NATURAL SELECTION hold the frequency of the gene in the gene pool?

The answer depends upon the selective advantage that heterozygous person has. If the selective advantage is very high, almost everyone without it will get malaria and die, then we would suspect that ½ of the gene pool would consist of the Hb_s allele. And humans would have to produce 4 offspring on average to get two viable ones to reproductive age (the homozygous Hb_s die from sickle-cell and the homozygous Hb_A [the normal allele] die from malaria).

Well, obviously malaria is a very bad disease but not everyone will get it, and not everyone who gets it dies before reproduction. So the selective pressure is not that great. The point at which natural selection will hold the frequency of the Hb_s allele in the population is the point where the selective advantage for being a heterozygote equals the selective disadvantage for being homozygote. It turns out that point will be where the per capita deaths from malaria within the Hb_A population will equal the per capita deaths in the Hb_s population.

Guess what! That is the point at which the frequency of the Hb_s allele is held in which populations in which malaria and sickle cell are endemic. What this shows then is that NATURAL SELECTION IS WORKING. And it is working EXACTLY the way we think it is. Thus, if natural selection can be shown to be working on this gene, then what is stopping it from working on every gene? Absolutely nothing! If it can cause this much a dramatic shift in the frequency of alleles in the population in a short time, what can it do by acting on alleles of a bunch of different genes over a longer period of time? There is absolutely no theoretical barrier stopping it from doing anything.

To make the point even more forcefully, let’s compare this with the creationist explanation. … Well actually they do not have an explanation. So we will use have to use their paradigm to come up with an explanation. Creationists say that “new information” cannot arise on its own. But with respect to malaria resistance the sickle cell trait IS new information. It causes infected cells to destroy themselves before they become a problem. That is novel information. So if this new information could not have arisen on its own, then an intelligent designer must have created it. But that creates problems … did the intelligent design not know that homozygotes would die from sickle cell disease? Could he not even foresee that simple problem? If that is the case then he is colossally stupid.

So who has the better explanation … modern evolutionary theory or creationism?

If this were an isolated phenomenon then I would say that it is not really important. But it isn’t. It turns out that evolutionary theory holds the explanation for the origin of a number of genetic diseases. For instance, heterozygotes for cystic fibrosis have a selective advantage in surviving cholera. We would never know this if it weren’t for research with an evolutionary paradigm to it.

Next, there are problems with the role of natural selection. In most evolutionary models, Natural Selection is given an almost creative role beyond what has been observed in nature. All that has been observed in both laboratory and natural settings is that of a conservative role for natural selection, with no evidence that it can do more than what we observed. Such assumption is hard to reconcile with actual science.

Er … what are you saying it should do … create its own variation? Well, in a sense it can even do that … see my section on evolvability above. One can think of natural selection as a sculptor, and the variation that is inherent in a population as the block of rock. When the sculptor starts, it is just a block of rock, but by winnowing away the bits and pieces of the rock, he can produce any work of art that he finds worthwhile. By winnowing away the variation in a gene pool, natural selection can create adaptations that are worthwhile for the reproductive success of organisms. That’s the role that scientists have ALWAYS said it could do, and that is the role that the evidence says it can do.

So, Gradual evolution, though, like most theories, this only scratches the surface, is now presented in as round and impartial way as I can present. There are whole books written on the topic and I could never hope to cover every scrap of information in this short blog, but it is my best idea of neo-Darwinism based on what I have been able to research.
If I have missed something, please post below what I have missed. Also note that nowhere in this series will I deal with abiogenesis, but rather will leave that to people who understand the theory better than I. I understand genetics and biology more than chemistry (I hated my chemistry class, although I was able to figure out the process of methanization without having encountered the theory before by just working out the encounters.

Despite this, I will mention that information theory is a vast and interesting subject for anyone to study. Next blog on this topic will be on punctuated Equilibrium, the theory brought forth by Gould.

I hope I have given you a LOT to think about (even if you didn’t make it all the way to here). I also hope you actually try to read some REAL science concerning evolutionary theory. But in any case it should be interesting to see what you have to say about Eldredge and Gould’s theory on punctuated equilibrium.

Cheers,

DB
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If a million people say a foolish thing, it is still a foolish thing. - Anatole France

In the bacteria, are there ever speciations? Or what happens to them if taken from the area of antibiotics? It isn't novel if it is just a defence. We have not seen a new species come out of those tests, so we have NOT seen anything novel. The likelihood is more that the gene(s) for resistance were already there in the first place, as it is with the moths in England (There has always been two types of pepper moths). Since you have NO proof that the variation was produced solely by way of mutation, then you have NO proof that the experiment resulted in a true novelty. The only thing you CAN say about that is that the population ratio changed, because that is the only thing you have proof of.

Secondly, you have no proof that the new information was not there already. We even have documents of people suffering from all the symptoms of sickle-cell anemia (that could be observed outside the body) from before the New Testament was recorded (And possibly even one within the New Testament as well, though that is speculation). how can you prove something is novel if it has been there in the homozygous state since before we encountered malaria or have records of people suffering from malaria?

Now, I have to go to a viewing, so you wait to educate me on something I haven't yet discussed until I have put forth all the theories. Don't assume what my creationary theory is until you have read it in my last blog.

PS: You would think that if I plan on doing a blog on Gould's theory that I would have some knowledge of species (multi-level) selection, founder theory and the rest of the theory.

In Bacteria, a species can be seen by it's changes in activity. Do the effects of the bacteria change? Does E. Coli ever change it's methods of attacking the body? If the only change is resistance to an antibacterial, then the answer, according to biology is a resounding no. You cannot tell me that they have designated them as anything other than separate strains of the same disease. Quit overexagerating the truth.

You don't get it, do you? There is still the major chance the gene was already there, and only a change in the system regulating the gene was triggered. It could be, oh my word, a defense mechanism. Quit pulling rabbits out of your hat and start pulling something substantial. It isn't novel if it happens every time you expose the organism to antibacterials and returns to the original set when you remove the antibacterial. It is like a yoyo. Novel means it hasn't happened before. next you'll be telling me that tadpoles changing into frogs is something novel.

What would "New" mean?

Definition from the American Heritage Dictionary:
Not previously experienced or encountered; novel or unfamiliar

and definition of Novel:

adj. Strikingly new, unusual, or different.

Now, if in tests prior to your test the same (or similar) result occurs (And there are several tests of this theory), then how would the later experiments be generating a novel response? If the response has occurred before in a lab test, it would stand to reason that it has happened and happens on a regular basis outside of the lab, where people, and the bacteria on them, encounter antibacterial agents both within and without the human body (medicines, soaps, etc.). Therefore, you have no reason to assume that it is a novel change, since it happens on a regular basis. It is not a different species. I might go so far as to call them a different strain of the same species, but not beyond that.

If you repeat the experiment, same antibiotic, same strain, and get the same result, would it be novel? or redundant?

how did you establish that EVERY SINGLE CELL had no resistance? If you had, then you would have a bunch of dead cells. There isn't a way to establish that every cell has no resistance. That would be like the Twelve Tribes Community assuming that there was never any child abuse going on in the community. Since scientists are humans, they cannot be fully sure of anything. But you are so fully sure that evolution occurred the way that the textbooks say it did, you don't question a thing the textbooks say. In fact, you won't even admit that it might just be an adaptation already in the organism that was activated after a threshold amount of certain chemicals in the antibiotics was reached. We have plenty of examples in the animal world and even in the human body where a response in the individual isn't triggered until a threshold has been breached. Examples such as the response of the pancreas releasing insulin based on the amount of glucose in the bloodstream, or endorphins being released when a threshold number of pain receptors are fired.

How did they prove, beyond the shadow of a doubt, that it is a genetic change (most likely a mutation of several dozen genes in an extremely unlikely and fortuitous series of mutations of the exact base pairs in the exact section of exactly the right genes) and not a response of the organisms that was built in already?

And, even if it was a genetic change, since mitosis OBVIOUSLY results in change of the dna (otherwise, there would be no point to the test), then you have no way of grabbing at which generation said change occurred, whether before or after the introduction of antibiotics, or even before the original cell was introduced. Because of the inherent unpredictability of mutation processes, you have no way to be completely sure of the time of the change, since mutations occur, most often, during mitosis, when the gene copies itself.