The theories of Creation & Evolution compared

[UTEOTW]

"2. Evolving from goo-to-you from molecule-to-human-brain requires "a massive decrease in entropy" according to Asimov - and yet all we "observe" is consistent overall "increase in entropy" in the local biological systems of mankind. This - Asimov says - IS WHAT the second law is all about."

Bob, why do you continue to quote Asimov as an expert, yet ignore your own experts explanation to you of why entropy is not a problem in the very part of the quote you cut out? Obviously you see that part as a problem or you would quote that part when you are quoting to keep the context in place. As is, it becomes just another example of quote mining to support an unsupportable assertion.

Of course you are also ignoring the last posting about how entropy has been shown to be a driving force towards life and not away from it.

"Self-Organization of Template-Replicating Polymers and the Spontaneous Rise of Genetic Information," Jarle Breivik, Entropy 2001, 3, 273-279.

Initially random sequences of monomers direct the formation of complementary sequences, and structural information is inherited from one structure to another. Selective replication of sequences occurs in dynamic interaction with the environment, and the system demonstrates the fundamental link between thermodynamics, information theory, and life science in an unprecedented manner.

This shows how entropy is a driving force in the formation of long chains from the simple building blocks and that this dynamic system leads to increased information. So this strikes at the heart of your arguments on both entropy and abiogenesis while also being problematic for Gup's assertions about information loss.

http://www.mdpi.org/entropy/papers/e3040273.pdf

 

[El_Guero]

WOW!

It will take me a little while to assimilate ... but, just remember, "resistance is futile" ...

In Christ,

Wayne

 

[UTEOTW]

While you are assimulating, I have another example of new information, this time by another process. In this case, parts of a gene for a pancreatic protein were used to make a new gene that makes "antifreeze" for cold water fish.

"Origin of antifreeze protein genes: A cool tale in molecular evolution," John M. Logsdon Jr. and W. Ford Doolittle, Proceedings of the National Academy of Science, USA,Vol. 94, pp. 3485-3487, April 1997.

Where do new genes come from? Duplication, divergence, and exon shuffling are the expected answers, so it is especially exciting when new genes are cobbled together from DNA of no related function (or no function at all). In this issue, Chen et al. (1) describe an antifreeze glycoprotein (AFGP) gene in an Antarctic fish that has arisen (in part) from noncoding DNA. Further, they show that a very similar AFGP from an Arctic fish is the product of some completely unrelated molecular processes (2). Together, these papers shed light on a number of key issues in molecular evolution.

In the late 1960s Arthur DeVries showed that freezing resistance in Antarctic fish was due to blood serum glycoproteins that lowered their freezing temperature below that of the subzero sea surrounding them (3, 4). The ensuing years have witnessed a great deal of work on AFPs (antifreeze proteins; not all are glycoproteins) in a number of phylogenetically diverse fish species, much of it by DeVries and his colleagues (5-7), revealing a number of types differing in their structure and amino-acid composition. These proteins, despite their diversity, function in similar ways to deter ice crystal growth (7, 8). But where did they come from, and how did they arise?

Birth of a Gene

In the first of the two papers, Chen et al. (1) demonstrate that an AFGP gene from the Antarctic notothenioid Dissostichus mawsoni derives from a gene encoding a pancreatic trypsinogen. The relationship of these two genes is not simply one of duplication and divergence (9), co-option/recruitment (10), or exon shuffling (11), processes that have been appreciated by molecular evolutionists for some time now. Instead, the novel portion of the AFGP gene (encoding the ice-binding function) derives from the recruitment and iteration of a small region spanning the boundary between the first intron and second exon of the trypsinogen gene (Fig. 1). This newborn segment was expanded and then iteratively duplicated (perhaps by replication slippage or unequal crossing-over) to produce 41 tandemly repeated segments. Nonetheless, the contemporary AFGP gene retains, as its birthmark, sequences at both ends which are nearly identical to trypsinogen. Retention of the 5 end of the trypsinogen gene may be significant, since this region encodes a signal peptide used for secretion from the pancreas into the digestive tract. Chen et al. (1) hypothesize that an early version of the notothenioid AFGP gene may have had its first function preventing freezing in the intestinal fluid, with this function later expanded into the circulatory system by way of its expression in the liver.

If you are curious, the reference for the other "antifreeze" mentioned is DeVries, A. L. & Wohlschlag, D. E. (1969) Science 163, 1073-1075.

Very interesting that we have not heard back from anyone yet showing how these examples are not really examples of new information. I guess because they are, in fact, new information no matter how you define it. New genes, new traits. And we have seen a number of different mechanisms.

 

[Gup20]

Unless you believe in some sort of Lamarckian evolution, no matter how many miles a day YOU ran, your CHILDREN would not receive a benefit.

Yet if a woman smokes during pregnancy, that is harmful to the unborn child and effects development. Strange how environmental factors such as diet, exercise, and in this case air effect biochemistry eh? Strange how something growing inside the mother could be effected in the same mannor as the mother eh? Wow. Astonishing. You really onto someting there. (rolling my eyes rignt now)

Neither I nor any prominent biologists believe in saltation. There is no such think as what you ask.

Evolutionists are leaning farther and farther towards quick bursts of evolution during the millions of years of supposed time. Why? Because multipart systems wouldn't arise simultaneously and there would be millions of creatures with useless vestigial organs/genes that would get 'selected out' before the whole system could develope according to that evolutionary model. This is another reason why finding out that non-coding DNA actually has a use - it debunks even further the opportunity for evlutionists to think this is leftovers or evolution in progress.

So no response to all this evidence for new information after all the claims that it is not possible?

Yeah... my response is you need to go back to the drawing board because your evolution theories are not credible... not by God's Word, nor be operational science. You STILL have yet to show a single example of information gaining process in matter.

 

[UTEOTW]

"Yet if a woman smokes during pregnancy, that is harmful to the unborn child and effects development."

Yes, environmental effects have influence on an unborn child. However, again, in this case the effect is passed on in a manner consistent with it being genetic. It is in the abstract. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=15353580&dopt=Abstract

Here we test the hypothesis that high-altitude native resident Tibetan women with genotypes for high oxygen saturation of hemoglobin, and thus less physiological hypoxic stress, have higher Darwinian fitness than women with low oxygen saturation genotypes. Oxygen saturation and genealogical data were collected from residents of 905 households in 14 villages at altitudes of 3,800-4,200 m in the Tibet Autonomous Region along with fertility histories from 1,749 women. Segregation analysis confirmed a major gene locus with an autosomal dominant mode of inheritance for high oxygen saturation levels, associated with a 10% higher mean. Oxygen saturation genotypic probability estimators were then used to calculate the effect of the inferred oxygen saturation locus on measures of fertility, in a subsample of 691 women (20-59 years of age and still married to their first husbands, those with the highest exposure to the risk of pregnancy). The genotypic probability estimators were not significantly associated with the number of pregnancies or live births. The high oxygen saturation genotypic mean offspring mortality was significantly lower, at 0.48 deaths compared with 2.53 for the low oxygen saturation homozygote, because of lower infant mortality. Tibetan women with a high likelihood of possessing one to two alleles for high oxygen saturation had more surviving children. These findings suggest that high-altitude hypoxia is acting as an agent of natural selection on the locus for oxygen saturation of hemoglobin by the mechanism of higher infant survival of Tibetan women with high oxygen saturation genotypes.

All the rolling eyes you want to give does not change the data.

"Evolutionists are leaning farther and farther towards quick bursts of evolution during the millions of years of supposed time."

And PE, saying that change happens rapidly on geologic timescales (read merely hundreds of thousands of years to millions of years) has what to do with saltation, the idea that "hopeful monsters" are behind change? Nothing.

"Because multipart systems wouldn't arise simultaneously and there would be millions of creatures with useless vestigial organs/genes that would get 'selected out' before the whole system could develope according to that evolutionary model."

Vestigal usually means something that no longer serves its original function. Either it does something else or nothing at all. And we do have a few vestiges just in humans.

We can look at the human body and see examples of where function is shared across species, has lost its original function, or has attained a new function.

First, the familar. We are all familar with animals puffing up their fur. Cats can do it to make themselves look bigger when frightened. Sometimes you will see animals do it in the cold to puff up the fur for greater warmth. Now look at you own arm the next time you are cold and feel goose bumps coming up. Or when something frightens you with the same reaction. We have hardly any body hair. Raising the hair on end will not keep us warmer nor will it make us look bigger. Yet we retain this function from our harrier past.

Can you wiggle your ears? Why? It has no benefit. At least to us. Our distant ancestors could turn their hears to help them hear better. Watch a dog or cat. (Not that I am saying they are our ancestors!) Some of us have not lost this ability.

Most of us are sitting on our bottoms. These muscles are huge (I think they may be the largest in the body.) and are essential to upright walking like ours. The other apes have the same muscle, but it is much smaller. This is why when you see a chimp ambling around on two legs they have that funny look where their knees are sharply bent with the thigh bones much closer to horizontal than in a human. Humans have devoloped this into a large muscle for walking but it is the same muscle as in the other apes. For that matter, look at the whole subject of upright walking. Our bodies have many problems because the bodies of our ancestors were on all fours. When moved upright, problems insue. Look at how many people have lower back troubles.

While talking about four legged ancestors... There is a muscle, the subclavius, that goes from the first rib to the collarbone. In other animals this muscle is used in moving the front legs for walking. Humans have not completely lost this relic. Some people maintain both of these on each arm, some only one, and some people none. They serve us no purpose.

Another muscle we no longer use is the plantaris muscle. This is used by other primates to grasp with their feet. We have no use for it and it has shrunk to the size of a nerve fiber.

There is a similar muscle in the lower arm called the palmaris. It is used by primates for hanging and climbing. In humans it has no function and is often taken by surgeons in need of a muscle elsewhere for reconstructive surgery.

"This is another reason why finding out that non-coding DNA actually has a use - it debunks even further the opportunity for evlutionists to think this is leftovers or evolution in progress."

Uh, actually... You wouldn't believe me if a told you.

http://www.binf.ku.dk/users/tlitman/binf/binf2kursus/Bioessays_2003_v25_p930.pdf

It appears that some of what we call junk is actually coding for RNA which seeks to regulate complexity in eukaryotes. This regulation is beginning to be thought of as the development that allowed for the rise of complex multicellular life and will turn out to be a key part of evolution. I just do not see how finding a use for some junk DNA is a strike against evolution. The genome is still littered with retroviral inserts and pseudogenes and all sorts of other stuff that are leftovers.

"You STILL have yet to show a single example of information gaining process in matter. "

Are you pulling my leg?

You gotta be pulling my leg. Really?

So a new version of a gene that allows a 10% increase in oxygen carrying ability is...a loss of information?

You have two genes near each other. They get copied at the same time. In one of the copies, the DNA between the two genes is lost and the two genes combine to make a new gene with a new function. And the old genes are still there. And this is...a loss of information?

A gene is duplicated. The new gene mutates until it can digest something the monkey was previously incapable of digesting while the old gene keeps its original function. And this is...a loss of information?

A virus inserts DNA into the host's genome. The DNA mutates and become useful to the animal (humans). This is...a loss of information?

A gene is duplicated and then a portion of the duplicate is then duplicated a few more times. The result is a new gene which makes a useful "anitfreeze" for the fish while the original gene remains. And this is...a loss of information?

I think you may need to address just why these are not increases in information but are actually decreases. They sure look like increases to me.

 

[UTEOTW]

I am afraid, after the last response, that I must ask again.

Tell us, in very specific terms, a scenario in which a mutation would result in new information in the way that you are trying to define it.

You have rejected all the ways I have given you for new genes to happen. Tell us how a new gene or a changed gene could come about that you would think is new information.

 

[UTEOTW]

While waiting for the above question to be answered, here is another bit of new information.

This is similar to the fish antifreeze gene but this time in a plant (carrot). A gene has been copied and a section duplicated repeatedly. The section that is repeated makes the protein rich in leucine. Another new gene with another new function. We have new information.

"A carrot leucine-rich-repeat protein that inhibits ice recrystallization," Worrall D, Elias L, Ashford D, Smallwood M, Sidebottom C, Lillford P, Telford J, Holt C, Bowles D, Science. 1998 Oct 2;282(5386):115-7.

 

[UTEOTW]

Well, we are still waiting for an answer to the question of a hypothetical mutation that would be accepted as new information*** and an answer to why the given examples are not new information although new genes and new functions have been evolved.

In the mean time, I'd like to give another example for the readers. In this case, we will venture a little bit towards irreducible complexity.

The bacteria Sphingomonas chlorophenolica uses a three step enzymic process to break down pentachlorophenol (PCP). Enzymes from other metabolic pathways were mutated and used to form a new metabolic pathway. One would think that a new metabolic pathway should be IC, but this little bug managed to accomplish this task and it is believed to have done so in the last few decades.

"Recruitment of a double bond isomerase to serve as a reductive dehalogenase during biodegradation of pentachlorophenol," Anandarajah K, Kiefer PM Jr, Donohoe BS, Copley SD, Biochemistry 2000 May 9;39(18):5303-11.

Tetrachlorohydroquinone dehalogenase catalyzes the replacement of chlorine atoms on tetrachlorohydroquinone and trichlorohydroquinone with hydrogen atoms during the biodegradation of pentachlorophenol by Sphingomonas chlorophenolica. The sequence of the active site region of tetrachlorohydroquinone dehalogenase is very similar to those of the corresponding regions of maleylacetoacetate isomerases, enzymes that catalyze the glutathione-dependent isomerization of a cis double bond in maleylacetoacetate to the trans configuration during the catabolism of phenylalanine and tyrosine. Furthermore, tetrachlorohydroquinone dehalogenase catalyzes the isomerization of maleylacetone (an analogue of maleylacetoacetate) at a rate nearly comparable to that of a bona fide bacterial maleylacetoacetate isomerase. Since maleylacetoacetate isomerase is involved in a common and presumably ancient pathway for catabolism of tyrosine, while tetrachlorohydroquinone dehalogenase catalyzes a more specialized reaction, it is likely that tetrachlorohydroquinone dehalogenase arose from a maleylacetoacetate isomerase. The substrates and overall transformations involved in the dehalogenation and isomerization reactions are strikingly different. This enzyme provides a remarkable example of Nature's ability to recruit an enzyme with a useful structural scaffold and elaborate upon its basic catalytic capabilities to generate a catalyst for a newly needed reaction.

emphasis added

***I understand why the question cannot be answered. An honest, intelligent answer to the question would open the door to a flood of examples that met the criteria. The best bet is to either continue to ignore the question or to maintain that all mutations no matter what are a loos of information. But, I think we have seen above that mutations are capable of generating genes that did not exist before that yield functions that did not exist before and that this can be accomplished in ways that leave the previous functions intact. If that is not new information, then the term is meaningless.

 

[Gup20]

All the rolling eyes you want to give does not change the data.

All the uniformitarian assumptions and pre-suppositions you have does not change the truth - which BTW is written in God's Word.

Are you pulling my leg?
You gotta be pulling my leg. Really?

Yep... I am pretty unimpressed by function in a gene that is designed for precisely that function. Clearly, the gene is designed to operate within that range and environmental or other factors may push it one way or the other towards the ends of the designed spectrum.... however... if the gene expresses function in that range without environmental pressure then perhaps the genes that determine regulation of that function based on environmental pressure is damaged. Natural selection determines that those with the benificial loss of information survive at a higher rate than those born without the ability to regulate that without stimulation who were born at the opposite range of designed specified operation tolerances.

This is analagus to a chocolate chip making machine. Lets say that machine can be set to make 100 chocolate chips per minute all the way up to 1000 chocolate chips per minute. If I walk over and see that it's set at 500 chips per minute... and I 1)remove the adjuster and hardwire it to 750, or 2)adjust the default level to 750 has the machine increased in information or gained specified complexity? No... the machine is doing exactly what it was designed to do... and within the range it was designed to do it. Same with the gene you referred to. It's doing what it was designed to do, and operating within known ranges (aka specified tolerances). That does absolutely nothing to show how you can go from molecules to man.

 

[UTEOTW]

"All the uniformitarian assumptions..."

Uniformitarianism is a part of geology, not biology.

"Yep... I am pretty unimpressed by function in a gene that is designed for precisely that function."

So a new version of a gene that allows a 10% increase in oxygen carrying ability was just part of the design of the original gene such that it would change through mutation in a beneficial way when the conditions warrented?

You have two genes near each other. They get copied at the same time. In one of the copies, the DNA between the two genes is lost and the two genes combine to make a new gene with a new function. And the old genes are still there. And these genes were designed so that this duplication and mutation could take place to give new function when the time was needed?

A gene is duplicated. The new gene mutates until it can digest something the monkey was previously incapable of digesting while the old gene keeps its original function. The gene's original function was to be copied and become something else?

A virus inserts DNA into the host's genome. The DNA mutates and become useful to the animal (humans). The DNA of this virus had the original function that it was to be introduced into the human genome, mutated into something beneficial, and spread throughout the population?

A gene is duplicated and then a portion of the duplicate is then duplicated a few more times. The result is a new gene which makes a useful "anitfreeze" for the fish while the original gene remains. So the duplication and replication to form a new function was a part of the original function of this gene?

"This is analagus to a chocolate chip making machine. Lets say ..."

I for the life of me cannot see how your analogy is supposed to be relative. It is an attempt to avoid answering the questions that you cannot answer.

Please tell me of a method of mutation that you would acept as giving rise to new information. Be specific.

Please tell me why, specifically, the above examples are not new information. I am not interested in some faulty analogy. Tell us specifically why the examples given, where new genes with new functions are created while in most of the cases the original genes is maintained to perform its original function, do not qualify as new information. I cannot see for the life of me how they cannot be.

And I do not think that you can either or you would have answered the questions directly.

 

[Gup20]

Uniformitarianism is a part of geology...

Ok... then tell me how evolution happened in 6000 years. If you do not take the uniformitarian assumptions of millions/billions of years, then please explain how we went from molecules to man in 6000 years.

Please tell me of a method of mutation that you would acept as giving rise to new information. Be specific.

There are no methods of mutation that increase information. All mutation re-arranges or decreases information.

You might as well ask which kind of grenades are good to use in treating cancer.

Please tell me why, specifically, the above examples are not new information

As I said before... I am unmoved by genes doing the exact thing they are designed to do within the range that they are able to do them. I bet if I started working out really hard, I could raise my own blood's oxygen carrying ability by more than 10%.

 

[Alcott]

I don't think I have ever posted on this general topic on BB before, and I suppose that is because I am no specialist or scientist, having taken no course in biology since high schooll; just chemistry and physics in college.

I am inclined to say that evolution does make sense and is a basis on which to form hypotheses, even though I have trouble believing it really happened as commonly theorized. But I have to base this almost totally on what I observe from a non-scientist's viewpoint. Wisdom teeth and the appendix are the most obvious physical examples of how it makes sense to assume we have the useless, and sometimes troublesome, organs from an ancient past which can be removed with nothing essential lost.

But what sometimes fascinates me considerably more than physical evidence that "we" have not always been as we are now, is the psychological angle. If you observe a group of children, such as class all about the same age, it doesn't take long to detect a "heirarchy" within the group. Some kid will be the #1, who most of the others defer to, and some kid will be the quietest follower. This #1 may be challenged, but if the challenger does not win, he will be obviously dejected and want to get away. I have seen this in animals, and it is apparent in a team of sled dogs or a herd of elk. Often, the one who gets to be #1 is the tallest, and we tend to expect tall people to be strong of character, and if they are not they will probably be ridiculed about their height, called "Stretch" or "Beanpole." Note that very few U.S. Presidents have been short.

Violence, racism, gang wars, selfishness/possessiveness, jealousy, boxing, Jerry Springer, and a lot more "base instinct" activities can be explained by this psychological angle of evolution. In choosing a mate, we consciously or subconsciously select one who looks like us and/or is the best-looking one who will have us, so that our children will also look good and look like us. If your church has a picture directory, take a look at the couples, especially the 'older' couples who have been together through so many years and notice the facial resemblences they have, which worked on them being attracted to each other in the first place. And where does the idea come from that the louder we say something the more true it is (we try that, don't we?)? Could it be that upcoming communication skills were, and still are, taking over from physical superiority?-- or louder = stronger? Words don't hurt us physically, but why do we so dislike our parents, bosses, et al, to "yell" at us? It's more than just sound, or it wouldn't be so unnerving or produce the negative feelings. We seem to be programmed to feel 'beaten' and experience the mental negativity of being physically beaten, even if it is only by words from 'authority.' Animals make threateing sounds and they are associated with the 'lesser' of the herd knowing they will be harshly physically dealt with if they don't 'obey.' Is this the relation we are making when we dread being 'chewed out?'

I don't want to be too explicit, but in spite of the modern feminist movement and so much talk about "sensitivity," it appears to me there are still few women who don't want a man who is physically strong, decisive, and authoritative. This seems to come from relating to a #1, or at least to the best challenger they can get. But while we've seen the #1 go from a gang leader of tribesmen to a big business executive, some of the physical characteristics of the old warrior chief are apparent in corporate success. My view may be limited, but most big execs seem to be big men who wear decisive expressions, have loud clear voices, and stand and walk tall. I even see this in the ministry; that pastors are taller than average, and people want their voices to be loud and authoritative and their posture and walk to be tall. Perhaps ironically, this image fits most of them who rant about the falsehood of evolutionary theory, when that might explain how they rose up in 'rank' and were deferred to as a #1 of the local tribe [church].

I am not conclusive as to whether evolution can explain these type of observations. But it does seem that God gave us a heritage with the mammals with whom we share the most genetic material, even if He did create us with such a heritage with no facts in reality behind it.

 

[UTEOTW]

"There are no methods of mutation that increase information. All mutation re-arranges or decreases information."

That line about rearraging is new. But I will get back to it.

You have just proven my entire point. You have chosen an arbitrary and capricious definition for information that has no bearing on the actual process of evolution. Your definition for information is chosen for convenience and through circular logic and is far outside the established definition for information in information theory.

There are quite a few examples given above (I can go for pages if you wish) of examples of novel genes with novel functions. The whole point of the YE argument over information is that evolution does not have a means to produce novel traits, at least not without giving something up.

Well, as shown, we have many examples of evolution doing just that. Evolution can add to the genome in ways that preserve existing function and create new functions that have never existed.

Your arbitrary definition notwithstanding, this is what is needed for evolution to proceed. New arrangements of DNA that code for new proteins with natural selection and other selective forces to determine which new genes make the creature more likely to pass on its genes to the next generation.

Furthermore, as suspected, under your definition there can not be any new information at all. If I were to sit down and write a novel, most people would consider that I have added to humanity's storehouse of information. But to you, I have not because all I have done is rearrange the words of the English language into a new order. No new information there.

"Ok... then tell me how evolution happened in 6000 years. If you do not take the uniformitarian assumptions of millions/billions of years, then please explain how we went from molecules to man in 6000 years.

First off, we are discussing biology. When you make such a comment and do not tie it to something else, then you appear to be commenting on biology. And uniformitarianism is not a part of biology.

Second, I have yet to see any reason posted not to accept the geology that indicates bilions of years. You have yet to show us a factual reason why we should expect that a geologic event or process in the past would be expected to leave a different set of effects than if the same event were to happen today. You have not demonstrated major problems in geology.

"As I said before... I am unmoved by genes doing the exact thing they are designed to do within the range that they are able to do them."

Did you read my examples? New genes that have never been in the gene pool before. New functions that have never been present in the organism before. Are you actually saying that part of the function of the genome is to evolve through various mutational processes? Maybe you do accept evolution.

" bet if I started working out really hard, I could raise my own blood's oxygen carrying ability by more than 10%."

But you could not pass that on to your children!!!!

Did you read the article? After accounting for all such environmental factors, there was a heritable change passed from generation to generation as a gene that allowed for the increased ability.

 

[UTEOTW]

Alcott

There are professional studies that echo what you have said. There is reason to believe that some behavioral traits have some basis in evolutionary history.

Some of the things you mentioned fall along the lines of sexual selection. I vaguely remember reading about some studies where they were able to show that men tend to pick women who are similar to their mothers and women pick men who are similar to their fathers when all other factors are taken into consideration. It is believed that some of the traits are passed on from generation to generation. For example, whatever traits that make a woman choose a husband who has certain physical and personality traits can be passed on to a daughter who would then be inclined to make a similar choice. It is not exact because personality and even physical appearance are mixtures of nature and nurturing. But there is a statistically significant relationship.

 

[A_Christian]

Behavioral traits find there roots in sin. When sin entered into the world through the sin of Adam the entire universe became contaminated and perverted.
This includes MAN's values, opinions, and investigations. Where GOD plays no part the effects are even worse and corruption becomes extreme.

 

[UTEOTW]

So you are saying that behavior is not heritable at all...?

 

[UTEOTW]

Well, while we await a response, I thought I would continue with another novel gene accomplished through the rearrangement of DNA. If may not meet the arbitrary YE definition of new information, but it allows for another new gene and so evolution proceeds despite contrary and factually baseless definitions.

"The Tre2 (USP6) oncogene is a hominoid-specific gene," Paulding CA, Ruvolo M, Haber DA, Proceedings of the National Academy of Science U S A 2003 Mar 4;100(5):2507-11.

In this case a gene went through a segmental duplication. The new segment was then combined with an old gene to form a new oncogene through chimeric fusion.

 

[UTEOTW]

This may be redundant if you are following the thread on the science forum.

http://www.baptistboard.com/ubb/ultimatebb.php/forum/66.html

I have another way for you to make new genes and functions even if some will still define it away as not counting as new information. What need does evolution have for a definition of "information" where new genes and functions can arise but still not be considered new information? It is an arbitrary and circular definition.

Anyway...

"The human genome contains many types of chimeric retrogenes generated through in vivo RNA recombination," Anton Buzdin*, Elena Gogvadze, Elena Kovalskaya, Pavel Volchkov, Svetlana Ustyugova, Anna Illarionova, Alexey Fushan, Tatiana Vinogradova and Eugene Sverdlov, Nucleic Acids Research, 2003, Vol. 31, No. 15 4385-4390.

http://nar.oupjournals.org/cgi/content/full/31/15/4385

In this case, existing DNA codes for mRNA that is then turned into cDNA through reverse transcription. This sequence is then permantently integrated into the genome by endogenous integration proteins. Basically a different way to copy a gene. This paper looks at a number of genes that have been created in this manner. Again, new genes and new functions.

But there is another interesting side to this. The evolution of the primates and apes can then be traced by when specific sequences were integrated into the genomes of the various common ancestors. When looking at this 12 specific chimeric retrogenes, you get the following chart.

http://nar.oupjournals.org/cgi/content/full/31/15/4385/GKG496F3

The distribution of the various genes in the various primates and apes, including humans, matches that which would be predicted through other techniques. That this technique matches that as done by other genetic, molecular and fossil methods is a very powerful combination of factors that strongly indicate the descent of humans from a common ancestor with the other apes.

This is very similar to the argument that can be made about retroviral DNA insertions. There are several insertions of viral DNA into the human genome. In a YE paradigm, you must assume that all these insertions happened in the very first generations but not since. This is because for us to all share them, they must have been in our last common ancestor. In a YE paradigm that would be Noah and there were only about 10 generations listed from Adam to Noah. Previously we have looked at the apes and primates on this subject. There we found that you can find the same sequences in the other apes and primates. So with these LTRs, you must not only assume that the human genome was very quickly littered with these viral inserts and then there were essentially no more inserts in the rest of the generations since, you must also assume that somehow the same combination of virii infected all of the other ape "kinds" (whatever they may be), inserted the exact same DNA sequences, that the sequences were spread to the whole populations of these different species, and that these insertions did not occur again later with such frequency if at all. Repeat this for the primates.

 

[UTEOTW]

Still no response on how we can be having all of these new genes and traits and it not count as new information. In the mean time, let's look at another mechanism through which new genes are made available for evolution to act upon.

We have seen how genes can be duplicated and one of the copies can then mutate to do something else. Well here is an even better method. Duplicate a whole chromosome and then you have lots of redundant genes that can start mutating into other things.

I give you

"The narrow sheath Duplicate Genes: Sectors of Dual Aneuploidy Reveal Ancestrally Conserved Gene Functions During Maize Leaf Development," Michael J. Scanlona, K. David Chenb, and Calvin C. McKnight, IV, Genetics, Vol. 155, 1379-1389, July 2000.

"The maize duplicate genes narrow sheath1 and narrow sheath2 encode a conserved homeobox gene function in a lateral domain of shoot apical meristems," Judith Nardmann1, Jiabing Ji, Wolfgang Werr, and Michael J. Scanlon, Development 131, 2827-2839 (2004).

Here maize has duplicated an entire chromosome and we seem to have caught the plant just as some of the genes start to differentiate into different roles.

The narrow sheath (ns) phenotype of maize is a duplicate factor trait conferred by mutations at the unlinked loci ns1 and ns2. Recessive mutations at each locus together confer the phenotypic deletion of a lateral compartment in maize leaves and leaf homologs. Previous analyses revealed that the mediolateral axis of maize leaves is comprised of at least two distinct compartments, and suggest a model whereby NS function is required to recruit leaf founder cells from a lateral compartment of maize meristems. Genomic clones of two maize homeodomain-encoding genes were isolated by homology to the WUSCHEL-related gene PRESSED FLOWER (PRS). PRS is required for lateral sepal development in Arabidopsis, although no leaf phenotype is reported. Co-segregation of the ns phenotype with multiple mutant alleles of two maize PRS homologs confirms their allelism to ns1 and ns2. Analyses of NS protein accumulation verify that the ns-R mutations are null alleles. ns transcripts are detected in two lateral foci within maize meristems, and in the margins of lateral organ primordia. Whereas ns1 and ns2 transcripts accumulate to equivalent levels in shoot meristems of vegetative seedlings, ns2 transcripts predominate in female inflorescences. Previously undiscovered phenotypes in the pressed flower mutant support a model whereby the morphology of eudicot leaves and monocot grass leaves has evolved via the differential elaboration of upper versus lower leaf zones. A model implicating an evolutionarily conserved NS/PRS function during recruitment of organ founder cells from a lateral domain of plant meristems is discussed.

From what I can tell, by studying where and how these two genes are expressed, they have found that each is evolving to function in specific and different roles within the plant.

 

[UTEOTW]

This is mainly to provide some support for my assertions about retroviral DNA insertions above. Again, if you are following the Science thread, this will be redundant.

"Constructing primate phylogenies from ancient retrovirus sequences," Welkin E. Johnson and John M. Coffin, Proceedings of the National Academy of Sciences of the United States of America, Vol. 96, Issue 18, 10254-10260, August 31, 1999.

Here, about a dozen different retroviral DNA inserts are used to construct the evolutionary tree of human and the other apes and primates. See the following chart to see how closely the different inserts match.

http://www.pnas.org/content/vol96/issue18/images/large/pq1892815002.jpeg

The genomes of modern humans are riddled with thousands of endogenous retroviruses (HERVs), the proviral remnants of ancient viral infections of the primate lineage. Most HERVs are nonfunctional, selectively neutral loci. This fact, coupled with their sheer abundance in primate genomes, makes HERVs ideal for exploitation as phylogenetic markers.
...
Endogenous retrovirus loci provide no less than three sources of phylogenetic signal, which can be used in complementary fashion to obtain much more information than simple distance estimates of homologous sequences. First, the distribution of provirus-containing loci among taxa dates the insertion. Given the size of vertebrate genomes (>1 × 109 bp) and the random nature of retroviral integration (22, 23), multiple integrations (and subsequent fixation) of ERV loci at precisely the same location are highly unlikely (24). Therefore, an ERV locus shared by two or more species is descended from a single integration event and is proof that the species share a common ancestor into whose germ line the original integration took place (14). Furthermore, integrated proviruses are extremely stable: there is no mechanism for removing proviruses precisely from the genome, without leaving behind a solo LTR or deleting chromosomal DNA. The distribution of an ERV among related species also reflects the age of the provirus: older loci are found among widely divergent species, whereas younger proviruses are limited to more closely related species. In theory, the species distribution of a set of known integration sites can be used to construct phylogenetic trees in a manner similar to restriction fragment length polymorphism (RFLP) analysis.

Emphasis added.

http://www.pnas.org/cgi/content/full/96/18/10254