Information applied to biology

[Administrator2]

[Administrator: the following is a combination of two threads, one after the other, dealing with information in biological systems. The second thread starts on the second page.]


GARPIER
This is an honest question in which I am only looking for a simple answer. Is it true that when a mutation occurs that there is a loss on genetic information?


DAVEW
I'm no expert, but the short answer is, not necessarily.

A point mutation involves one genetic "letter" being changed to another. No net loss of information, but if that "letter" was part of a "word" that is now nonsense, you could say information is lost (conversely, if a point mutation transforms a bit of nonsense into a word, information is arguably gained).

A deletion involves (duh) genetic material being removed and not replaced. Again, this would seem to involve a loss of information, but possibly the deletion makes sense out of nonsense.

I'm pretty sure that there are cases of additions, where extra stuff gets added. Again, this is an increase in genetic material, but not necessarily in "information."

There are other forms of mutations (frameshift mutations, etc.) that basically scramble the information around without adding material.

At any rate, most mutations are either neutral or harmful (either because they cause loss of information or addition of "bad" information). But there are some undeniably beneficial mutations. I think this is being discussed in another thread, and there's something with bacteria and plasmid transfers that is being described as a beneficial, information-adding mutation.


RUFUSATTICUS
Every mutation actually adds information. This is perfectly obvious when you remember that populations evolve not individuals. (Well, for sexual organisms at least. ) Mutations add new 'information' to the gene pool of the population. As Darwin pointed out, evolution cannot happen without variation. Mutation is the primary source of variation.

One might observe a "loss of something" when comparing an organism to its parents. But, when looking at the population, something is gained because there is now a new individual with a unique combination of genes.

-
GARPIER
Are you saying that in my genes that there is more genetic information than there was in my grandparents genes or just that the information in mine is different than the in theirs?


DANEEL
As has been pointed out by another person in this thread when talking about information and mutations the concept of the gene pool is more useful in understanding exactly what is going on. It's not the individual but the total gene pool that changes as genes are passed from one individual to another through time. Mutations which are less adaptive will not be passed on as readily as those that increase fitness. So information is constantly changing and being reorganized in new forms. Given enough time with duplication of genes and chromosomes natural selection has more and more genes to work with. The mutation rate, generation time, population size, the environment , time and other factors are involved. Evolution is not simple in the details.


RUFUSATTICUS
Are you saying that in my genes that there is more genetic information than there was in my grandparents genes or just that the information in mine is different than the in theirs?


The latter.
If you compare the information of your grandparents' generation with your own, you will see that the information it contains differs from the information in your generation. Which one has/had more information? Probably your generation since it is larger. Likewise the generation of your grandchildren will have more information than yours. (Assuming no WWIII. )


FROGGIE
Hee hee hee. I guess no one told you that you can't use genetics and simple in the same sentence. Kind of like government intelligence (j/k--hey I work for big brother! )

The 'simple' answer is, it depends on what type of mutation you are referring to, and where that mutation occurs.

We'll first consider point mutations, like an A converting to a G during DNA replication. Some mutations result in the same protein sequence (three or four DNA 'letters' often translate to the same amino acid, like changing a Q to a q in UBB--the function is the same). In this case, there is no gain or loss of info.

In many cases, a mutation will cause a "loss" of information. For example, a patient with cystic fibrosis has only one less functional protein than you or me, but this has dire consequences for their lung function and their health.

There are a couple of ways that mutations can result in a net gain of information. For example, if a promotor sequence gets mutated (the switch that turns a gene on or off), theoretically it could mutate such that a new pattern of transcription factors act on it. This would be new information.

Gene duplication during unequal crossover is a huge source for a mutation causing new information. This phenomenon occurs during meiosis in our sperm and egg cells (well for me only in egg cells ). The chromosomes will duplicate and line up on the cell axis, ready to be separated into two new cells. But while they are waiting around, their arms will actually swap. It mixes up our mom and dad's DNA, which provides one more level of diversity….

Imagine if a gene like hemoglobin (the oxygen-carrier protein in our red blood cells) gets duplicated in an ancestral vertebrate. If one of them mutates to lose function, no harm done (you still have one good copy). But what if the new copy mutates to become a better oxygen carrier? Now you could evolve a mammalian system such as pregnancy. Babies developing in the womb use a different form of hemoglobin than adults, so they can get enough oxygen from their mother's blood. (This is of course what molecular biologists think happened in hemoglobin evolution).


HRG
In many cases, a mutation will cause a "loss" of information. For example, a patient with cystic fibrosis has only one less functional protein than you or me, but this has dire consequences for their lung function and their health.

If the mutation which makes this protein non-functional has never occurred before, it is certainly an increase of the information contained in the gene pool of a population. Arguing about the functionality of proteins confuses information with meaning, IMHO.


GARPIER
Have their been any mutations observed which added genetic information or material?


FROGGIE
Observed in our lifetimes? Yes. Remember however that you aren't going to see huge changes in our lifetimes, which accd to ToE is very small compared to the age of the earth and the total time that evolution has had to work on RM&NS.

Here's an interesting tidbit I just read in the article entitled, "Coding sequence evolution," by Kreitman and Comeron, Current Opinion in Genetics and Development, 1999, vol 9, page 637-641. They were talking about some interesting work done by Dean and colleagues. They are researching biochemical pathways, which are similar to developmental pathways (highly regulated, depend on environment and genetics, etc). Here's a snip of the article:

Dean and colleagues investigated an ancient evolutionary change in isocitrate dehydrogenase that shifted the enzyme from being NAD-depended to being-NADP-dependent. This evolutionary event, it is argued, allowed an ancestor of modern eubacteria to utilize acetate as a carbon source, thus opening up an immense new ecoogial niche for bacterial exploration. By [using X-ray crystallography and mutation analysis], they identified six amino acids that together could cause a shift in preference of IDH from NADP to NAD. Two additional changes allowed the modified E coli enzyme to function at comparable levels to the eukaryotic NAD-dependent enzyme...in this manner these authors were able to infer the sequence of the ancestral IDH and to elicidate likely changes that occured over three billion years ago to bring about this major adaptation!

Here's an abstract of some of the work. I found this quote quite interesting:

Another abstract has this to say:

Guided by x-ray crystal structures and molecular modeling, site-directed mutagenesis has been used to systematically invert the coenzyme specificity of Thermus thermophilus isopropylmalate dehydrogenase from a 100-fold preference for NAD to a 1000-fold preference for NADP. The engineered mutant, which is twice as active as wild type, contains four amino acid substitutions and an alpha-helix and loop that replaces the original beta-turn. These results demonstrate that rational engineering of secondary structures to produce enzymes with novel properties is feasible.

All mutations are harmful and do not produce any new or novel mechanisms? I don't think so!


HELEN
I think there may be a problem here with the word 'information.' No one has defined what they mean. Rufus, for instance, is referring to stochastic, or random information, which is applicable only to Shannon information theory (which deals with compressibility and does not concern itself with meaning, sender, or receiver).

However that is not what is going to work in genetics. As far as a living organism goes, genetic information has to be meaningful. The addition of random bits here or there has the same general effect in the cell as adding them to a fine watch would have -- gums up the works.

In order for the cell to continue functioning any added 'information' must have meaning, must integrate into the genome without disturbing the other functions, and must be understood and 'obeyable' by the cell in one way or another.

Here is a rough -- very rough -- picture. The organelles and tissues in the cell are the army. The nucleus is the general. The orders the general gives have to make sense to the soldiers involved and they must be able to carry them out. If the general says 'advance', they know what that means and they can do it. If the general says 'blurb', that may be added bits of 'information' in terms of what they are trying to process, but it means nothing. They do not understand it and they can't obey it. If the general says 'fly', they can understand the meaning, but they cannot flap their arms and obey it. The orders must be appropriate to the function of the cell and be understood. Dropping or adding to the letters in the words would normally only remove actual meaning, which is what I think garpier is actually referring to when he talks about information.

So, do mutations mean a loss of meaning for the genome? Very often, yes. Most mutations do not seem to affect the life processes or replication of the cell. Those that we are aware of that DO affect the cell (and thus the organism), mostly either switch around information or drop it -- meaning that in both cases meaning is dropped whether or not any structure on the DNA is dropped or not. When a bit of the DNA manages to replicate itself in double, is this added information? No, in neither the Shannon nor the meaningful sense is this added information!
Shannon information increases with novelty, not with repetition. Meaningful information increases with meaning itself.

So if a sequence is running 'abcdefg' and 'efg' appears a second time, no information is added, for there is nothing novel there. In the same way, exchanging places or dropping something from the genome does not increase information either, in either sense, UNLESS there is something which the cell can respond to which it could not respond to before, which has been facilitated by the change.

What evolution depends on is the increase in meaningful information, which is said to occur through random mutations. Meaningful information could be increased through a simple change in start or stop codons or the larger change in a gene sequence itself which would either change its function or invalidate it. Sometimes the latter might conceivably be of use to the organism.

What is generally seen, however, is that mutations involve meaning loss -- and, in that sense, information loss.

RUFUSATTICUS
For the record, I hate the word 'information.' It is does not translate well into genetics, IMO.
Helen,
Any mutation is a change in information for an individual; this adds information to the population. How do you tell the difference between a 'loss' and 'gain' of information? You seem to be claiming that a 'loss' adversely affects the cell. Well, I can imagine situations where a loss of function is benificial to an organism. (Light skin near the poles.) The converse could also be true: situations where a gain of function is harmful to an organuism.

If a sequence is running 'abcefg' and 'efg' is added, there is definately new information added. 'Abcefgefg' does not contain the same information as 'abcefg.' If you duplicate 'not' in a sentance you can have an entirely different meaning. Despite being duplicated, information is still added.

Evolution requires inheritable variability in a population. That is why any mutation adds information. Mutations produce novel genes and combinations. If a mutation is harmful, evolution will sort it out. If it is beneficial, it'll become more prevelant in the populaion. The point is that every mutation adds information to the population and evolutionary forces filter that information into the next generation.

KC
Originally posted by garpier:
This is an honest question in which I am only looking for a simple answer. Is it true that when a mutaion occurs that there is a loss on genetic information?

Not always. We know this because some mutations revert back to the original wild type. If a reverse mutation like this was a loss of information, how could it revert back to the original?


GARPIER
Not being a scientist, a lot of this information is hard for me to follow let alone understand. So I'll cut to the chase. I understand that there may be mutations within organisms like bacteria and there may be mutations in multi-cellular organisms as well. But from what I,ve been able to understand the result is a mutation of what ever that organism started as. For example the mutation of a bacterium results in another bacterium. I guess this is called micro evolution. But has there ever been a documented mutation of one type of organism into a different type of organism or macro evolution?


KMGRABA
Macro-evolution FAQ: http://www.talkorigins.org/faqs/macroevolution.html

29 Evidences for Macroevolution: http://www.talkorigins.org/faqs/comdesc/
[Administrator: please note that this is the original of an ongoing exchange with Ashby Camp
http://www.trueorigin.org/theobald1a.asp
http://www.talkorigins.org/faqs/comdesc/camp.html
http://www.trueorigin.org/ca_ac_01.asp ]

Speciation: http://www.talkorigins.org/faqs/faq-speciation.html

More Speciation: http://www.talkorigins.org/faqs/speciation.html


DAVEW
Garpier, bacteria existed on the earth for a good half-billion years before developing from prokaryotes to eukarotes (presumably through endosymbiosis -- do a web search on "endosymbiosis" for more info). It's hardly surprising that bacteria observed in labs for the past roughly 100 years would fail to demonstrate the kind of "macroevolution" you demand.


GARPIER
I didn"t demand anything. I asked if there had been any obsereved examples of macro evolution. If the answer is "no" then just say so.

kmgraba,
Thanks for the links, but I didn't see anything about observed mutations resulting in macro evolution. Did I miss it?


KMGRABA
A single mutation will not always lead speciation (or "macroevolution"). However, I think there are a few mutations which can lead to speciation, such as gene duplication in plants. Section 5.1.1.1 of the Speciation FAQ looks to be one example.

[ January 18, 2002: Message edited by: Administrator ]

 

[Administrator2]

MR BEN
A published paper detailing experimental evidence which supports the assertion that mutation + natural selection not only produces new information, or 'specified complexity', and also easily produces 'irreducible complexity'.

Evolution of Biological Information http://www.lecb.ncifcrf.gov/~toms/paper/ev/ev.pdf
[Administrator: this is a pdf file with a very long load time]

2794–2799 Nucleic Acids Research, 2000, Vol. 28, No. 14 © 2000 Oxford University Press
Evolution of Biological Information
Thomas D. Schneider

National Cancer Institute,
Laboratory of Experimental and Computational Biology

ABSTRACT
How do genetic systems gain information by evolutionary processes? Answering this question precisely requires a robust, quantitative measure of information. Fortunately, 50 years ago Claude Shannon defined information as a decrease in the uncertainty of a receiver. For molecular systems, uncertainty is closely related to entropy and hence has clear connections to the Second Law of Thermodynamics.
These aspects of information theory have allowed the development of a straightforward and practical method of measuring information in genetic control systems. Here this method is used to observe information gain in the binding sites for an artificial ‘protein’ in a computer simulation of evolution. The simulation begins with zero information and, as in naturally occurring genetic systems, the information measured in the fully evolved binding sites is close to that needed to locate the sites in the genome. The transition is rapid, demonstrating that information gain can occur by punctuated equilibrium.

From the articles conclusion...

The ev model quantitatively addresses the question of how life gains information, a valid issue recently raised by creationists 32) (R. Truman, http://www.trueorigin.org/dawkinfo.htm ; 08- Jun-1999) but only qualitatively addressed by biologists (33). The mathematical form of uncertainty and entropy (H = –?plog2p, ?p = 1) implies that neither can be negative (H ? 0), but adecrease in uncertainty or entropy can correspond to information gain, as measured here by Rsequence and Rfrequency. The ev model shows explicitly how this information gain comes about from mutation and selection, without any other external influence, thereby completely answering the creationists.

The ev model can also be used to succinctly address two other creationist arguments. First, the recognizer gene and its binding sites co-evolve, so they become dependent on each other and destructive mutations in either immediately lead to elimination of the organism. This situation fits Behe’s (34) definition of ‘irreducible complexity’ exactly (“a single system composed of several well-matched, interacting parts that contribute to the basic function, wherein the removal of any one of the parts causes the system to effectively cease functioning”, page 39), yet the molecular evolution of this ‘Roman arch’ is straightforward and rapid, in direct contradiction to his thesis.

The 'ev' program, written in PASCAL simulates the coevolution of protein binding sites. These sites evolve over time using simple mutation (inversion, duplication) and selection. The change in information content is mapped as the simulation progresses, and the the speed of information growth is measured. The simulation is directly analagous to how natural biological evolution occurs.


JOHN PAUL
Wow a real live computer simulation! Gee whiz Mr Ben and here I thought you had some real evidence.

According to Claude Shannon's definition of information 1 pound of gold has the same value as 1 pound of sand and random characters have the same information as the same number of letters that form meaningful sentences. Shannon's definition was only to test the transmission, reception and storage of data. To use it as a measure for biological information is very deceptive.

That said I got a good chuckle out of the ending sentence (just before the acknowledgements):

"So contrary to probabilistic arguments by Spetner (32, 33), the ev program also clearly demonstrates that biological information, measured in the strict Shannon sense, can rapidly appear in genetic control systems subjected to replication, mutation and selection.(33)"

For anyone interested in what Spetner has to say:

A scientific critique of evolution http://www.trueorigin.org/spetner1.asp

The dialog continues http://www.trueorigin.org/spetner2.asp


MR BEN
Wow! A Real live computer message! Gee whiz Mr Paul, and here I thought you had a real rebuttal.

I agree. It is obvious that computer simulations can tell us nothing about the processes of evolution. After all computers are not biological organisms, thus they can tell us absolutely nothing about 'biological' evolution.

Likewise, it is obvious that the English language can tell us nothing about 'biological' evolution. English is not a biological organism, therefore any statement written in English is invalid in terms of any arguments expressed for or against evolution.

Likewise, it is obvious that mathematics is not a biological organism, therefore we can rule out mathematics as well.

Likewise pencils, pens, computers, email, webpages, etc. Anything that is not a biological organism can be safely ruled out as being useful in a discussion about evolution. If a statment was written with a pen, that statement is invalid. If it was communicated in english, it is invalid. If it describes a mathematical forumula, that formula is invalid. etc. etc.


According to Claude Shannon's definition of information 1 pound of gold has the same value as 1 pound of sand and random characters have the same information as the same number of letters that form meaningful sentences.

That is actually the opposite of what shannon said. The measure of information is the difference in entropy in a set of symbols in coding system that differs from the maximum entropy expected by random chance selection of symbols.

The minimum information content of a sequence is the number of bits required to represent that sequence in a specified code with the minimum redundancy. When we are talking about biological organisms, it is the number of bits required to represent protein coding genes, or more restrictively to represent protein coding genes with measurably different phenotypic effects.


Shannon's definition was only to test the transmission, reception and storage of data. To use it as a measure for biological information is very deceptive.

DNA is a means of storage of genetic data, biological process are a means of transmission, reception, and in the case of evolution, generation of this data.

The coding system of DNA is well known. Random sets of DNA do not code proteins.. only a finite set of sequences code actual working proteins. Of this set, only a finite set code proteins with real measurable phenotypic effects. An increase in bits coding proteins with phenotypic effects not seen before in an organism in unarguably an increase in the specified complexity of that organism.

Spetner has unilaterally decided to define 'information' as not only the coding in the genes which which exists now, but any coding changes that could occur in the immediate future. Thus no amount of genetic change we can observe could change Spetners 'information content'.

If an organism evolves a receptor capable of making it more virulent, Spetner simply says that the 'capability' to evolve that new protein was part of the 'original' information of that organisms, and thus no information content change.

Taken to extremes, we could say that the capability of early Ungulate precursor mammals to evolve into whales was simply part of their original microevolutionary capability, and thus no net 'specified information' content increase or even change.

Spetner also argues that "most" mutations that lead to bacterial resistance is a 'loss' of information. This is simply not true. First of all, often this resistance is accompanied by an 'increase' in the coding DNA for a protein, introducing new novel codons. Secondly, there is almost always an increase in 'meaning', i.e. a protein now not only carries on its original function, but it also aquires a new phenotypic effect, namely resistance to one or more antibiotic receptors.

From Spetner:
Max cited gene duplication as an example of a mutation that increases information. A favorite scenario for molecular evolution is that a gene gets duplicated and then gradually mutates to become something useful that did not exist before. Such a proposed scenario does not constitute evidence for evolution, it proves nothing, and indeed such a scenario itself requires proof. I do not, of course, mean to say that one has to prove that genes can be duplicated. That is well known. But gene duplication alone does not constitute an increase of information in the biocosm or even in the genome of the organism itself. Two copies of today’s newspaper contain no more information than one copy. Gene duplication, in any case, cannot play the role of the mutations that could produce the grand sweep of evolution.

This is not true, it contains one more bit of information... the fact that Spetner now has two newspapers instead of one. This information might be pretty important if he had only subscribed once, and was being chanrged twice, or if he simply didn't want to get two papers delivered to him every day.

Just because the 'content' of the newspapers did not change, doesn't mean that having two of them does not change the state of the entire system. Likewise, a repetition of two coding genes can have a substantially different effect on an organism from a phenotypic viewpoint. Where as one copy may have one effect, having TWO copies may have a substantially different effect.

Technically, I think any 'repeat' is an increase in information of log2N where n is the number of repeats.


ECORI
i'm curious as to whether the following example would count as an "increase in information". if not, why not?

a strain of bacteria that contains a penicillin resistance gene on a plasmid is cultured in the presence of a weak mutagen, then plated onto petri dishes that contain both ampicillin and penicillin (note plasmids are circular pieces of DNA that can be present in multiple copies in one bacterium). colonies that grow on the dishes are cultured, then their DNA extracted and their penicillin resistence gene sequenced. in some colonies, the bacteria contained two sets of plasmids. one contained the original penicillin resistance gene, the other contained a mutant copy of the gene which conferred resistance to ampicilin.


MESK
This is definitely an increase in genetic information, and an undeniably beneficial mutation to boot. But you'll need a peer-reviewed reference to back it up - do you know where these results were published?



HRG/ALTER EGO
I submit that one need not measure the information in a gene to know if a particular mutation has added or subtracted information. There is no general way of measuring the information in a single message without relating it to the ensemble of messages from which it was chosen. Similarly, there is no general way of measuring the entropy in a single message without relating it to the ensemble of messages of which it is a member. Shannon was careful to avoid relating the information measure he was defining to the meaning contained in a message.

There are two points to be said.
First, the ergodic theorem relates time-averages to ensemble averages. If a single message is sufficiently long, the entropy we can calculate it will approximate the entropy calculated from the statistical ensemble of messages to any desired accuracy.

Second, no meaning is ever inherently contained in a message. Meaning always requires a decoder (which does not have to be intelligent, of course).


FROGGIE
Lol! Sorry, I am not purposely laughing at you Mesk. But--well, knowledge about plasmid transfer between bacteria is in nearly every micro textbook. I'm sure there's a really old reference though!


MESK
Hi froggie,
Just a few points, if I may.

Firstly, with all due respect, you misinterpreted ecori's post. The increase in information he was postulating was not due simply to the transfer of plasmids, but to the generation of a novel ampicillin resistance gene via mutations in a pre-existing penicillin resistance gene. There's no reason why the reference couldn't have been relatively recent.

Secondly, you misinterpreted my response. I was not asking ecori for evidence out of contrariness, but rather because I expected that his creationist opponents would demand it (which, it turns out, they didn't).

Thirdly, you appear to have misjudged my beliefs. I'm not a creationist. I have in fact been arguing the case for evolution on the web for several years.

And finally, your accusations of ignorance are misdirected to an amusing extent. As quite a few of the people on this board know, I used to work in microbiology, albeit in a relatively junior position. I now work on the molecular biology of muscular dystrophy, and given that I've spent much of the last week actually transferring plasmids into bacteria (I'm trying, without much success, to clone splice isoforms of a muscle gene) I found your comments particularly ironic.


ECORI
the example i gave earlier was hypothetical. i just wanted to make clear whether or not the example would count, before i spent the hour or two on pubmed and at the library looking up the references. i'm fairly certain that the amp resistance gene came about through random mutation of the the original beta-lactamase gene conferring penicillin resistance. but i really hope it's not as easy as the experiment i described earlier. if it were, we'd all be in trouble!


MESK
It sounded clear-cut enough to me, but I expect creationists will demand the following:

1. Proof that the initial bacterial population did not possess ampicillin resistance or any version of the amp resistance gene. (This is not as straightforward as it might seem. Many studies of this type start with a clonal bacterial population derived from a single antibiotic-sensitive bacterium; unfortunately, most studies don't state this fact explicitly, so expect to be challenged on it.)

2. Unambiguous (and preferably multiple) sequence differences between the initial penicillin resistance gene and the novel ampicillin resistance gene, with definitive evidence that it is in fact the mutant gene which is conferring ampicillin resistance.

2. Spotlessly sterile experimental conditions, so that the possibility of horizontal transfer from another bacterium is eliminated. Don't expect to be able to satisfy this demand. Standard aseptic technique will not satisfy the creationists - there is always a chance that the amp resistance gene originated from a contaminating amp-resistant bacterium, and no amount of duplicates and replicates will convince them otherwise.

If you can find a reference that satisfies all these demands, my hat goes off to you. See, I know that bacteria can generate novel antibiotic resistance genes through simple mutation and selection - I've seen them do it myself. But I've never been able to find a reference that can prove it to the satisfaction of creationists (surprise surprise). Maybe a thorough and intense literature search could do it, but frankly I'm too lazy.


ECORI
i agree. part of my frustration when researching the literature stems from the fact that the authors are not trying to prove their results to creationists, so there are a lot of things they take for granted (like naturalism), that a creationist would claim is debatable. but before i venture into that arena, i'd like to know from the creationists on this board what would count as a gain in information. they always like to pick some obscure feature like a new organ, when they know full well that evolution does not claim that new organs appear de novo. (incidently, does anybody know what organs a human possesses that a mouse doesn't? i sure don't)


JOHN PAUL
they always like to pick some obscure feature like a new organ, when they know full well that evolution does not claim that new organs appear de novo.

From what did organs evolve? Please substantiate your answer with evidence.

[ January 18, 2002: Message edited by: Administrator ]

 

[Administrator2]

THE BARBARIAN
From what did organs evolve? Please substantiate your answer with evidence.

From pre-existing structures. Let's take insect wings as an example.
Insect flight evolved about 330 million years ago.
Genetic studies show that wings evolved from articulated gills on aquatic insects. Pre-existing structures were simply reworked to a new function.
(Carroll, Weatherbee, and Langeland, 1995; Averof and Cohen, 1997).

How?

"Modern stoneflies walk on the surface of water, and raise their rudimentary wings if they feel a puff of air. They then get propelled across the water by the breeze (Marden and Kramer, 1995). Some species even stand on their hind limbs and flap their wings as they sail" (Kramer and Marden, 1997).

References:
Averof, M., and Cohen, S.M. (1997) Evolutionary origin of insect wings from ancestral gills. Nature, 385, 627-630.
Brodsky, A.K. (1994) The evolution of insect flight. Oxford: Oxford University Press.
Carroll, S.B., Weatherbee, S.D., and Langeland, J.A. (1995) Homeotic genes and the regulation and evolution of insect wing number. Nature, 375, 58-61.
Kingsolver, J.G. (1985) Butterfly engineering. Scientific American (August), -97.
Kramer, M.G.,and Marden, J.H. (1997) Almost airborne. Nature, 385, 403-404.
Marden, J.H., and Kramer, M.G. (1995) Locomotor performance of insects with rudimentary wings. Nature, 377, 332-334.


JOHN PAUL
Insect flight evolved about 330 million years ago.
Genetic studies show that wings evolved from articulated gills on aquatic insects. Pre-existing structures were simply reworked to a new function.

This is what I found, which is slightly different from what you posted:
"Insect flight evolved about 330 million years ago. There is genetic evidence that wings evolved from articulated gill plates on the limbs of aquatic ancestors, rather than being novel outgrowths from the body wall (Carroll, Weatherbee, and Langeland, 1995; Averof and Cohen, 1997)."

Then we should be able to experiment on this. We should be able to take an organism that has gills, make the appropriate genetic changes and see if wings replace the gills.

BTW, what is this genetic evidence?

But then we would have to show, genetically, how gills arose. Can you do that Pat?


HRG/ALTER EGO
Do we have to ignite a supernova in our lab in order to establish the astrophysical theory of supernovae ?
Please tell me well in advance before you plan such an experiment


JOHN PAUL
Do we have to ignite a supernova in our lab in order to establish the astrophysical theory of supernovae ?

Be my guest.
The point is until we have direct observational data of a star collapsing and then going nova or supernova, all we have is our thoughts on how the process works. Our thoughts could be right on the money but until we substantiate them... Well you get the idea.


JAYCWRU
We have no direct observation of atomic structure. Should atomic theory go out the window because of this?
Seeing isn't a criteria for science. There are countless ways to observe and study physical phenomena.
Lets throw this back at you. If life is ID, did you get a chance to observe the designer? You don't have a direct observance of life being designed don't you? So why is ID a more plausible "theory" than the ToE.


JOHN PAUL
We have no direct observation of atomic structure. Should atomic theory go out the window because of this?

We have direct observations from experiments we have done involving atoms. That is what lead us to today's atomic theory.


Seeing isn't a criteria for science. There are countless ways to observe and study physical phenomena.

So are you saying observing isn't seeing? Interesting.
Science is only as good as the scientists conducting the research and those who review it. That is why theories change


If life is ID, did you get a chance to observe the designer?

Not that I remember. But I didn't have to see my car, computer or TV being designed to infer they were designed.


You don't have a direct observance of life being designed don't you?

Again, not that I remember.


So why is ID a more plausible "theory" than the ToE.

Because where in nature do we see specified complexity arising via purely natural processes?

Here's the link you didn't want: Why Evolutionary Algorithms Cannot Generate Specified Complexity http://www.discovery.org/viewDB/index.php3?program=CRSC&command=view&id=10

Ya see I understand that science is done through inference. That is not a problem for me. What is a problem is when people run around claiming the inference is fact.


FROGGIE
So I'm not exactly a mathmatical expert. But I see no formula in this Dembski paper that I would call even adecent model for an "evolutionary algorithm." Where is the forumla that accounts for gene duplications, transversions, insertions, deletions, alternative promotor usage, alternative splicing mechanisms, or integration of viral genomes? I saw no mathmatical formula anywhere that contains even one of these evolutionary mechanisms, much less all of them.

Every single probability argument I've ever seen that addresses the "improbability" of evolution NEVER addresses these genetic and epigenetic phenomenon. Why? Because we are just now figuring these things out, and the best geneticist in the world doesn't know how to mathmatically model these things.

Remember--most of the evidence for evolution was figured out before genetics. Darwin himself was at a complete loss to explain "how" these 'heritable factors' caused evolution. Many people were not convinced of evolution for that very reason. Then genes were discovered, which explained how natural selection could have occured. Of course even in the 1950's after the characterization of the structure of DNA, there were still a lot of unanswered questions. But then scientists kept discovering strange things like jumping genes and retroviruses, which further explained the likelihood of evolution.

It seems like every hole that is pointed out in evolution is eventually filled by scientific discovery. I was just reading a national geographic article this morning about whale evolution. The author stated that whales used to be a poster child for creationists, because scientists did not have enough explanations for how whales evolved. But now many more fossils have been discovered and whales are one of the best examples of evolution.


JOHN PAUL
The author stated that whales used to be a poster child for creationists, because scientists did not have enough explanations for how whales evolved.

Now you may have an explanation but still nothing to substantiate that explanation. That is what Creationists want- something to substantiate the claims made by evolutionists.

As for genes and DNA, these were not predicted by the ToE. Once we found them ID should have been thrust to the forefront. That it wasn't shows me to what lengths evolutionists will go to in order to save their materialistic naturalism PoV.


MR BEN
But I didn't have to see my car, computer or TV being designed to infer they were designed.

Living organisms are NOT TV's, Cars, or Computers. Manufactured objects do not remotely resemble organically replicating biological organisms.

Now wasn't this the same argument you were using against computer simulations of evolution. Ironically, in this case this particular argument is justified, because it is the differences between manufactured and replicating objects that is the 'key' difference.

So why is ID a more plausible "theory" than the ToE.


Because where in nature do we see specified complexity arising via purely natural processes?

Wanna guess? Living organisms, of course. That's not the only place we see specified complexity arising from chance mutation. Computer simulations progress much faster and are easier to analyze.

[regarding the link to Dembski’s article] Dembski didn't even address the real evolutionary algorithm. He simply talked about directed optimization (i.e. Dawkins NON-evolutionary algorithm based on "Methinks it is like a weasel". Dawkins never stated that this example was an evolutionary algorithm, but a demonstration of how retained correct guesses can quickly lead to that particular sentence. Evolution is an undirected process, and simply finds the first nearest solution amongst many possible solutions.

Dembski's argument is based on a false premise that evolution starts with a copy of the genome, and matches random guesses to a known final result. This is a cartoon version of evolutionary algorithms that he mistakes for the real one.

Finally, Dembski ignores all of the recent study that has gone into complexity theory and emergent systems. The physical laws of chemistry and physics, along with the replication of a genome, make such a complex system, and specified complexity is an emergent property of such a system.


FROGGIE
Heritable factors were indeed predicted (and proposed by darwin). They just didn't know what the darn things consisted of. Evolutionists knew that in order for the theory of natural selection to work, there had to be some sort of heritable unit or factor (which contradicted with the Lamarckian idea of heritable-ness for lack of a better term). People were still skeptical in Darwin's day because that heritable factor was not characterised or identified yet. Now it is, and genetics makes perfect sense in the context of evolution.

You still never answered the main part of my post, BTW. Where is the ID explanation/mathmatical model for gene duplications, transversions, insertions, deletions, integration of viral genomes, alternative promotor usage, and alternative splicing? TOE has explanations that make sense and make predictions. Do you?

In case anyone still believes that TOE did not predict genes, here's some stuff from talkorigins to prove how wrong that statement is:

The Development of Evolutionary Theory
Biology came of age as a science when Charles Darwin published "On the Origin of Species." But, the idea of evolution wasn't new to Darwin. Lamarck published a theory of evolution in 1809. Lamarck thought that species arose continually from nonliving sources. These species were initially very primitive, but increased in complexity over time due to some inherent tendency. This type of evolution is called orthogenesis. Lamarck proposed that an organism's acclimation to the environment could be passed on to its offspring. For example, he thought proto-giraffes stretched their necks to reach higher twigs. This caused their offspring to be born with longer necks. This proposed mechanism of evolution is called the inheritance of acquired characteristics. Lamarck also believed species never went extinct, although they may change into newer forms. All three of these ideas are now known to be wrong.

Darwin's contributions include hypothesizing the pattern of common descent and proposing a mechanism for evolution -- natural selection. In Darwin's theory of natural selection, new variants arise continually within populations. A small percentage of these variants cause their bearers to produce more offspring than others. These variants thrive and supplant their less productive competitors. The effect of numerous instances of selection would lead to a species being modified over time.

Darwin's theory did not accord with older theories of genetics. In Darwin's time, biologists held to the theory of blending inheritance -- an offspring was an average of its parents. If an individual had one short parent and one tall parent, it would be of medium height. And, the offspring would pass on genes for medium sized offspring. If this was the case, new genetic variations would quickly be diluted out of a population. They could not accumulate as the theory of evolution required. We now know that the idea of blending inheritance is wrong.

Darwin didn't know that the true mode of inheritance was discovered in his lifetime. Gregor Mendel, in his experiments on hybrid peas, showed that genes from a mother and father do not blend. An offspring from a short and a tall parent may be medium sized; but it carries genes for shortness and tallness. The genes remain distinct and can be passed on to subsequent generations. Mendel mailed his paper to Darwin, but Darwin never opened it.

Too bad for Darwin! If he had read Mendel's works, well. . . maybe people would have been convinced much faster of his theory and. . . ok no more speculation for froggie. Too depressing to even think about.

[ January 18, 2002: Message edited by: Administrator ]

 

[Administrator2]

[Administrator: from another, related, thread:]


BWSMITH
Will wrote: what is the mechanism for information increase in DNA? I realize we have seen examples of information decrease within species but what about increase?

The key to your question lies in your definition of "information". Are you simply equating "length of the nDNA strand" with "amount of information"? If so, mutations go both ways, leading to both insertions and deletions in the total linear code. Most of these changes are innocuous (the vast majority of the human genome doesn't do anything for us), but some help and some hurt the organism. The ones that help get reproduced.

Also, change in genetic structure is not always accomplished through simple basewise mutations. The study of the human genome shows that sometimes viruses that insert their own genes expedite the process of radical genetic change for us on a larger scale than simple base-by-base mutations. However, both simple mutations and large-scale gene infections still fall under the umbrella of "explainable by natural processes", though.


If you believe as most neo-Darwinians do, that it is mutations combined with natural selection, how do you account for the development of complex systems (i.e. the eye), in such an undirected system?

Be careful. It IS a directed system. Eyes come from "proto-eyes". Better and better vision over time is rewarded under natural selection. Complexity results from increasing reward as that complexity gives increasing benefit.


Also doesn't the finding of master control genes, such as Eyeless, cause you to question mutations developing such systems?

No. Why would it? (Such a question implies that you associate progressive "mutations" with chaos.)


Talk Origins presents the classic evolutionary tree, however doesn't it really look more like a confused bush

It's not by any means a "confused" bush, but a bush nonetheless. The "bush" model is a better visualization than the traditional, simple tree, yes.


with the findings of the master control genes? After all these genes were shared prior to eyes being developed.

The master control genes expedited the process of eye development. They themselves were also the product of evolutionary change.


Isn't the only evidence for evolution homology?

What do you mean by the "only evidence"? If we reduce all organisms to their original DNA strand and compare those, then their homologies give understanding of the relationships between them. However, the present state of organisms is only one part of the equation. How homologies change over time is the other. The fossil record, among other things, fills in some of the general picture of what generally came from what.


Can't that be interpreted 2 different ways?

Yes. God could have created us with all our homologies fully intact, and we would expect to be able to compare genes and see similarities and differences. It's when we look back in time to see what change took place over what time periods that we begin to diverge from a literal reading of Genesis.

It's at that point that we must be absolutely positive that the way we interpret Genesis is the way it really should be interpreted. It turns out that it isn't; inerrancy is a late Protestant doctrine that was not supported by the early fathers. Higher criticism gives us a path for better understanding what Genesis is really saying under the motivation that it apparently was never intended to be a science book.