Jim, Macro evolution has been observed in the laboratory under controlled conditions – within just a few generations you can “breed” fish to be miniature fish, which reproduce and “grow” up while never getting bigger than the size they were bred for. And Jim, I NEVER said that belief in evolution in inconsistent with a belief in God. I am merely saying that the case for evolution is overwhelming and cannot be denied by any rational person who bothers to examine the evidence. Belief in God is based on faith, not evidence; and it would be entirely appropriate to believe that evolution, like the other laws of the universe, are merely the hands of God shaping the world we live in. As for referring to evolution as “intelligent design”, I would have to agree – there can be no more intelligent a design program than the evolution that created the amazing diversity of life on this planet including mankind himself.

“Er” I’m a PhD biologist myself James, and I’ve been studying evolution for 25 years. Evolution is a result of the combination natural selection (and yes, in the lab it would be artificial – same thing except in nature you have to wait until conditions change so selection is usually slower) AND speciation. Speciation is a much more complicated process that occurs on a much slower time scale. By definition (when two sub-species can no longer productively interbreed to create a group that can reproduce) – however, things are more complicated than that! As any biologist will tell you, the devil is in the details – some “speciation” can be a result of behavior – two subspecies may no longer ever mate due to changes in mating behavior and/or geographic separation. Others are due to cytogenetic changes – while a donkey and a horse are genetically 99+% identical at the gene sequence level, the cytogentic changes make their common hybrid (the mule) generally sterile (non-dysjunction during gamete formation), EXCEPT in a very rare cases where the chromosomes happen to align in just the right formation – there are a few documented and proven cases where mules were able to effectively cross-breed with horses or donkeys. Horses and donkeys are far down the speciation path so sexually reproductive hybrids are extraordinarily rare. Zebras show an intermediate cytogenetic phenotype/structure between those of horses and donkeys, and as such their progeny (zebroids) have much greater success at matings with either parental species. The “mules” for lion-tiger matings (ligers and tigons) are fairly functional reproductively and can fairly readily interbreed with their parent species (so much more like the zebroids), so these are less far down the speciation path, even though tigers and lions are still considered different species. There are examples of interspecies hybrids that can reproduce, thereby creating a hybrid species. This shows cases where the two species are even more closely related. One example is the American Red Wolf, which is a hybrid between the Gray Wolf and the Coyote. (There are other know cases too.) And finally there are sub-species which don’t generally mate, but can and when they do they produce offspring that can mate with either parental species or their own hybrid-type; examples of this would be Bengal and Siberian tigers mating or Kodiak bear or Grizzly bear matings with Polar Bears. The time-scale require for speciation is much greater than that for natural selection, but is the aspect of evolution that drives speciation (essentially ‘nails down’ the changes that build up over time in sub-species, and starts preventing backcrosses from homgenizing the two species). These cytogenetic changes are much like those that occur in all animals during the early stages of somatic cancers, but of course only the most conservative changes can be heritable (any gametes with the more significant cytogenetic changes would not survive development). So as you can see James, while it is not feasible to reproduce the ‘slow’ aspect of evolution (cytogenetic speciation) in the laboratory (because of the great time scales required), there is a wealth of evidence of how this process occurs in the natural world around us – showing species and sub-species at all levels of speciation. There is an extraordinary wealth of proof of evolution not only at the fossil level (which is dramatically greater than the state 20 years ago, the supposed “holes” creationists point to no longer exist), but also now at the genetic level (as many extinct species have had their genomes sequences with new high-throughput sequencing techniques, many within just the last couple of years), and this information complements and clarifies the fossil data wonderfully. And here I’ve told you about examples of speciation that are currently ongoing in the world today, and they are present in a wide range of levels. Anyone with a biology background who claims to see no evidence of evolution is being willfully blind!

And Jon, you can put whichever “label” you want on it, model or theory, I don’t really care – either way it’s happened throughout the natural history of this world, and it continues to happen today.

read it again, there’s an extensive outline of the paleontological, genetic, cytogenetic evidence. If you can’t understand it, let me know the part you can’t understand and I can explain it to you.

I just explained to you “speciation”, which is the basis behind macro-evolution. I showed you how different species can sometimes mate (Canis lupus can mate with Canis latrans – two different species – and produce offspring that can reproduce with themselves), I explained as you move farther away evolutionarily the species can hybridize and hybrids show some, but decreasing ability, to successfully mate as the species are more distantly related (are you going to tell me lions are tigers, or zebras are horses or donkeys?) I pointed out how a macroevolutionary experiment cannot be done in the laboratory because of the time frame required for cytogenetic changes to occur (do you know what those are?). So unless you can provide a time machine, those experiments cannot be completed for many lifetimes. But that doesn’t mean that you can’t evaluate and measure the genetic and cytogenetic changes that are in the midst of occurring throughout the world in the many examples I’ve given of species, sub-species, and closely related species showing every step along the way toward speciation. In spite of your readings, you seem to lack some basic understanding of not only biology, but how to objectively evaluate biological data. But I guess that’s the case isn’t it – reading the Bible does not make one a minister, reading biology books does not make one a biologist, anymore than knowing an opera by heart makes one a opera performer. Reading something is different than the skill set to actually DO it. I am a biologist trained (and hired) at some of the best institutions in the world – I don’t write the textbooks, I do the research that ends up being written about by textbook authors.

re-read!!! – I never said “macro” evolution could be observed. I was referring to the microevolutionary changes. When you brought up macro I started telling you about the cytogenetic changes required for speciation or macroevolution. Both steps, micro and macro, are required for evolution. Pay attention!

Man, you are not a very astute student are you?

Yes, according to your own citation above, lions and tigers are separate species. As I stated above. Very good Sean.

I disagree with the very opening aspect of this text. As I cited before while Great Danes and Chihuahuas cannot breed it is only due to physical limitations – artificial insemination would result in a perfectly viable mutt. This is no different than two sub-species which do not interbreed only because they’re on different canyon ridges and do not cross the canyon. This text is ‘popular’ science, it is not a text used by scientists. Some things are misleading.

Macroevolution does NOT require an “increase in the gene pool” – the gene pool of the horse and donkey are virtually identical, yet they are separate species (yet closely related enough to produce sterile offspring). The reason they are different species is due to the cytogenetic changes (note that does NOT involve additional genetic material or a greater gene pool).

My apologies for the lack of clarity on my part. When this thread first started we were talking about common evolution in the lab. This is commonly seen with microorganisms. Someone asked what about non-microorganisms. I responded that you could see macro evolution in the lab in fish (macro just to differentiate from micro-organisms). Once you began defining your terms as micro and macro evolution as being the small changes due to variation and selection, versus the larger changes that produce different species that of course made my previous point unclear – I was referring to micro-evolution (variation and selection) being studied in a macroorganism (fish). It wasn’t an over-reach, it was a miscommunication due to us not having established an accepted nomenclature prior to that statement. Often different branches of science will utilize the same term to mean different things in different fields. As to your question of which fish – Atlantic silversides. Here’s the website showing you the surprising result that within just a handful of generations the fish size could be decreased dramatically. http://evolution.berkeley.edu/evolibrary/article/0_0_0/conover_04

….Once you defined what you were discussing through the terms of micro versus macro evolution, all of my other statements made still stand as written

….As to your longer question about evolution above and how it relates to species and higher orders. There are many elements you have of confusion there. One simple one that makes me concerned is that you state a chihuahua has “much less specified complexity” amongst the Canids. Not at all true! It’s complexity is just a great, but everything has just been bred to be on a smaller scale – larger doesn’t inherently mean more complexity Sean.

As for your comment about my conflating species with genus or family – that is exactly my point Sean! The very definition of evolution is the creation of new species. The formal definition of a species is that it cannot interbreed and create viable young with another species. Yet we know of several cases where that does indeed occur – you give some examples yourself Canis lupus and Canis familiaris. Whereas most species do follow the rule that they cannot interbreed with others at all. There are other genuses or even families of organisms where there is still some interbreeding that can occur, but their ability to produce offspring vary – and I gave you examples of different species of bear that can produce viable offspring, but different species and even genuses of the horse family that can produce offspring with varying degrees of ability to interbreed successfully. I have even given you some information on why these various equines produce progeny of differing ability to interbreed – their speciation is being driven by cytogentic changes – in the cases of this group horses, donkeys and zebras all have very similar genetics (about 99% of their genes are the same) yet those genes are divided up amongst a different number of chromosomes (donkeys have more smaller chromosomes, horses the fewest larger chromosomes, zebras are intermediate in number and size). These cytogenetic differences are what limits production of offspring with a full ability to reproduce (due to nondysjunction during meiosis, production of gametes). And these are the type of cytogenetic changes that, as I was describing earlier, over time begin to prevent back-crossing, which allows the microevolutionary changes (like those we see with the fish) to over time become more permanent, driving the diversity of the evolutionary tree. My point has been that all these examples show speciation at different stages: while wolves and dog, or wolves and coyotes, are different species (by most criteria), they can still produce viable offspring – they have not truly become fully independent species as per the formal criteria; bears are somewhat similar as polar bears can produce viable offspring with Kodiak bears and grizzly bears and North American brown bears, any offspring produced with European brown bears do not survive to adulthood – speciation was achieved between polar bears and European brown bears, but is incomplete between polar bears and North American brown bears; equines are a third example, where all three discussed, horses, donkeys and zebras – which belong to not just different species, but even different sub-genuses, can produce offspring, but those offspring cannot interbreed successful, and have varying ability to produce offspring with the parent species (donkey-horse, extraordinarily rarely, horse-zebra or donkey-zebra, much more often) – so the equines are much further down the speciation path than Canis or Ursid, yet not nearly as far as some species which cannot produce offspring at all. So THIS Sean, is macroevolution – no one would say a polar bear is the same species as a grizzly or a brown bear – yet they are only partway along the path to speciation. Similarly donkeys and zebras are clearly not the same species as horses, yet these are further along the way to speciation. These are the examples where I’m showing you that evolution is occurring in the here and now, and that we can see different groups of animals at different stages of speciation. This is the best we can do in describing the individual steps in macroevolution as we cannot carry out speciation/macroevolution in the laboratory because of the time frame required to generate stable cytogenetic changes in organisms – selection can occur over just a few generations, cytogenetic changes occur over generations upon generations.

Dr. Catchpoole is an expert neither on evolution nor on genome integrity (one of my fields of expertise). He is not qualified.

And you’re wrong again, resistance to antibiotics is due to a GAIN of genetic material, not a loss. You talk a good game Sean, but the fact is that you don’t know enough facts about basic biology to support your thoughts. This is what we need to explain to college students who figure that once they read a text and can pass an exam, they must be experts; and why can’t they just do whatever they want in life (being an expert on something) because they can always ‘find’ the answers they need online or in a book. The problem is that you need a solid basis upon which to build – if you don’t have the basic material you really can’t support your ideas and arguments. (kind of like needing to have a vocabulary of words before you can write a paper). You Sean have collected a great number of books and ideas, but you don’t REALLY know the science behind what you’re talking about – which leaves your theories and positions full of holes/flaws. It’s been an interesting discussion but I can’t continue this indefinitely – I have work to do. If you don’t understand the concept that evolution is a continuum of small changes and selections, punctuated by larger cytogenetic changes that prevent back-breeding, ultimately leading to speciation (different species). And if you can’t understand how all I’ve shown you supports both aspects of that – then I suggest you head back to school for a degree in Biological Sciences – you clearly have the interest.

No Sean, your last comment is very wrong. It wasn’t their advanced degrees in other areas that make them capable in other things. In each case those individuals had to study and learn a whole new area to become capable. Furthermore, development does not always come from an expert – some people do not full understand what they develop or contribute to. Invention does not always come from the greatest knowledge.

That’s actually not true either Sean – are you saying that the genetic information in a wolf contains that of the chihuahau, but not the reverse? That’s not true at ALL. You don’t understand basic genetics. Selective breeding over enough time can create either from the other.

Okay Sean, finally have a few. In response to your posts above about purebred dogs losing genetic diversity and bacteria – those statements you have reposted have elements of truth, but are written in a misleading fashion (whether purposeful or due to lack of understanding I have no way of knowing, so will not judge). It is true that purebred dogs have lost genetic diversity (variation) – but they have NOT lost genetic material. This is due to breeders continuing to backbreed to select for rare or desired traits. Note this also sometimes selects for genetic problems; as I’m sure you are aware many purebreeds have serious problems – just like humans have problems when backbred (why we have traditions and even laws against very close blood relatives marring and having children). But that loss in diversity is not due to a loss of genetic material (not due to a loss of genes). It is mutations, or slight changes in genes, that cause genetic diversity. This might alter their function, or might even turn the gene all the way off in some cases (Mexican hairless?). So yes, purebred dogs have lost genetic diversity, but all the genes required for them to be a wolf are still there! It would take probably hundreds of years of breeding to re-select for those wolf-characteristics, and some of the small mutations in genes that affect their function would have to re-arise, but it could and would happen. The genes ARE still there.

Bacterial selection for antibiotics: for bacteria the situation is a bit different. In addition to their bacterial chromosome, bacteria often also have extrachromosomal DNA that they can pick up from the environment or other bacteria, and that they can pass on to their progeny. Antibiotics generally act against basic physiological pathways that bacteria need to duplicate their DNA, make RNA, synthesize their bacterial proteins, or synthesize their cell walls, among others. As you can imagine stopping any of these processes will stop bacterial cell growth. Antibiotic resistance is not due to a loss of any bacterial genes. In some cases it may be due to some small mutation in a bacterial gene that leaves the protein encoded by that gene still functional, but changes the shape just enough that the antibiotic no longer binds effectively, so no longer works. More often bacteria pick up some DNA (whole genes) from the environment or other bacteria around (and these might be other types of bacteria that do not cause disease) that give the bacteria resistance to the antibiotic. Usually these antibiotic resistance genes act one of two ways: one is the gene may encode an enzyme that breaks down the antibiotic (common with penicillin-resistance); the second is that the gene may encode a molecular pump that pumps a variety of small molecules like antibiotics out of the bacteria. If the bacteria is continuously pumping the antibiotic out, the antibiotic is not effective. So in the case of bacterial antibiotic resistance, again there is no loss of genetic material, actually there is a gain of genetic material.

What these posts don’t recognize is that even when there is a mutation, this is NOT a loss of genetic information! It is a loss of diversity, and possibly function (or altered function). But the gene is still there – and it can be mutated back to full function just as easily as it mutated to lose function.

Also it is obvious why bacteria isolated from soil or from many years ago have these genes, penicillin was discovered in naturally occurring mold. This is in the environment, and some bacteria throughout natural history have had to deal with this as well as related molecules – so these enzymes and molecular pumps in some specific environments would be selected for over time. As we use antibiotics in healthcare (and sadly in animal feed), there is more selection for bacteria to pick up and hold onto these genes. That’s why they’re more prevalent in our environment than they were fifty years ago.

[….]

Oh, Sean, I forgot. As for how these antibiotics like beta-lactamase or antibiotic pumps arose though evolution. You can look at the amino acid sequence of these proteins and there are some very closely related proteins in some bacteria that are used for different purposes – they break down something other than beta-lactamase and pump other molecules into or out of bacteria. What has clearly happened is that these genes were duplicated and random mutations occurred. At some point in time, one or more of these mutations led to subtle changes in the protein which made it function in a new way – so that it could break down beta-lactamase (the ring in the penicillin structure). This then provided that bacterium with a selective advantage when it was in an environment with that family of mold. This idea of gene duplication is quite common – we humans also have gene duplications throughout our genomes. Most of these are not expressed and not currently “used” if you will – so don’t provide us any advantage now – but appear to be the place where new genes/functions can arise. There are cases where past pseudogenes have evolved to be used. There are several copies of human hemoglobin. In some other animals only a single hemoglobin is used, and the other copies remain as unused pseudogenes. In humans we still have some unexpressed hemoglobin pseudogenes, but we use more than one hemoglobin; at least one is only expressed and used in utero, and is developmentally turned down (to about 3%) as we are born and mature – then the standard hemoglobin is the primary hemoglobin. It is unclear what advantage the fetal hemoglobin provides in utero, but this is the way we have evolved. We guess there is some advantage to using it.

[….]

Okay. But even I would say that all by itself acquisition of antibiotic/pesticide resistance is not evidence for evolution. It’s just one very small brick in a very large wall. It’s consistent with evolution, but by itself it’s just one tiny piece of evidence. If it wasn’t for all the other evidence for evolution, then this by itself might be one little weird anomaly

[….]

“In his book Not by Chance, Spetner likens this situation to the disturbance of the key-lock relationship. Streptomycin, just like a key that perfectly fits in a lock, clutches on to the ribosome of a bacterium and inactivates it. Mutation, on the other hand, decomposes the ribosome, thus preventing streptomycin from holding on to the ribosome. Although this is interpreted as “bacteria developing immunity against streptomycin,” this is not a benefit for the bacteria but rather a loss for it. Spetner writes:

This change in the surface of the microorganism’s ribosome prevents the streptomycin molecule from attaching and carrying out its antibiotic function. It turns out that this degradation is a loss of specificity and therefore a loss of information. The main point is that Evolution… cannot be achieved by mutations of this sort, no matter how many of them there are. Evolution cannot be built by accumulating mutations that only degrade specificity.”

This is only partly correct Sean. These mutations that occur in the bacterial chromosomal genes that confer resistance to streptomycin (there are more than one that have been discovered) do indeed alter the structure of the ribosome (the enzyme complex that synthesizes proteins). But they do NOT “decompose the ribosome” as Spetner claims. If they did, the bacteria could not survive, as all bacteria (and larger life forms) require protein synthesis to survive! While these mutations alter the bacterial ribosome somewhat, so streptomycin does not bind, the mutant ribosomes still have enough structure to function. In the absence of streptomycin long-term bacteria with this mutation would be out-competed, as they’re not quite as efficient at protein synthesis – but they’d survive just fine in mixed populations without strong selective pressure. Also, as I said above, there is nothing to prevent these single point mutation from mutating back to the normal “wild-type” configuration in the absence of streptomycin. It doesn’t happen any more efficiently than the original mutation to streptomycin-resistance, but it doesn’t happen any less efficiently either. I’m actually shocked at Spetner’s statements you posted – it shows a clear lack of understanding of basic first year microbial biology! I’m kind of appalled.

Sean, the point I made above, about how some of the things Spetner states are just plain wrong, makes me question his deductive powers. There are similar things in the sections you’ve posted above. He’ll take one correct point, and then follow it up with a second statement about it or a conclusion about it which is patently wrong! Because he starts with a correct statement, you start giving him credence (and it sounds like he knows what he’s talking about. But then he screws it up completely. I can’t even bear to read the little pieces you’ve posted he because he’s made such a mashup of some correct facts, some incorrect statements, and completely fallacious reasoning – I sorry, I just can’t bear to read his work. His reasoning is just garbage – as I’ve pointed out in the example I gave above.

Point mutations, like the one he describes about Streptomycin, do not “degrade specificity”. They ALTER specificity – and might even bind other things BETTER than the original. Because he uses the words “degrade” and “loss of genetic information” (I pointed out above how that conclusion of his is wrong too), it SOUNDS like his conclusion makes sense – that this “loss of specificity” and “loss of genetic information” could not be a positive for evolution. The problem is his characterization of those mutations as being a “loss” of information is simply incorrect. This is what I was talking about above, where he makes a point that is correct – a mutation can caused decreased binding to streptomycin – but his descriptions after that are incorrect and misleading. Virtually everything you’ve posted by him is like this – he starts with one correct statement, then makes misleading or mischaracterizing statements about it, allowing him to build a fallacious argument. One of two things – either he doesn’t know what he’s talking about, or he’s trying to mislead you – I don’t know which.

It’s interesting Sean, I actually agree very much with that point made above “Any scientist with an agenda is not a scientists but a poor philosopher with dangerous intent…. God is beyond being “proven” or “disproven”, which is of course inherent for a being all-powerful. It is beyond any man to prove or disprove God.” – this is actually something I teach my students VERY hard – to not become wedded to a theory, to be willing to let that theory go WILLINGLY, if the data argues against it. I have no agenda here – I neither want to prove nor disprove God (such attempts are silly, if we accept God is all powerful, it is beyond the power of Man to prove or disprove). I only want to look at the data and see what they indicate. I would argue VERY STRONGLY that the scientists you have been posting have an AGENDA – and that agenda is to disprove evolution. Ergo, as per your post above – they are very poor scientists. And based on their writings that you’ve posted, I agree wholeheartedly – their writings are rife with errors and mis-conclusions. Conversely I do not believe that believing in Evolution precludes an all-powerful God. Much of the Bible is written as parable or allegory, and I believe that Genesis is written in much this way – written in a way so mankind at that time could comprehend what was written. So unlike most, I go into the Evolution question with an open mind, without any goal or either proving or disproving God. So if you put that question aside, and ask what the data supports, the data overwhelmingly supports Evolution – otherwise why would there be so many fossils of species showing intermediate forms between ancient life forms and current life forms, otherwise why would gene homologies across both current species as well as compared to ancient species show incremental changes consistent with Evolution. Instead of you probing my knowledge and ability to support Evolution with the biological systems in the world – let me ask you a question. If God created all the species currently on the Earth either 6000 years ago, or through intelligent design, why is there so much evidence that supports Evolution? Why Ancient species, why evidence for intermediate species? If you believe in an all-powerful God, yet don’t believe in Evolution, then why are these fossils there, then why does the genetic code show evidence of intermediates and sequence-relatedness consistent with Evolution? Do you believe God put it all there just to try to confuse us? Seems like a lot of trouble just to play a little mind-game with mankind – ??