Subject: Re: Teaching science Re: Op-Ed: Why evolution is still correctly called a theory Date: 7 February 2005 Message-ID: firstname.lastname@example.org
Robert Grumbine wrote:
> >This sort of ignorance is exactly why I begin each semester with an
> >anlysis of what is, and is not, "science".
> I make it one of my early labs when I teach astronomy.
> How do you teach it or about it?
I found that I had to teach the nature of science at both the undergraduate and graduate levels for the honors class and molecular genetics class that I taught. Even at the graduate level the understanding of science cannot be taken for granted. It turned into my one lecture spiel. I'd hand out essays by Richard Feynman and Peter Medewar on the nature of science for the students to read and then we'd work on a jigsaw puzzle. I'd use the puzzle as an example of how science works. I'd use those cheap 100 piece kid puzzles that you can buy at Wal-Mart. I found that the two puzzles that I purchased had an identical cut out pattern with different pictures.
The first thing that we'd do is turn over the pieces and I'd try and get the students to think about the problem. Just looking at the pieces, can they come to some sort of idea of what the picture was. Unless you have some type of super genius that can assemble the pieces in their mind the students can only come up with vague ideas of what the picture might be. We do this in science all the time. Even the assumption that it will make a picture that they can make sense of should be pointed out to them. Try and get them to think about what they are doing. When they start to assemble the puzzle ask them what they are doing. None of the students I've had have tried the random assembly of just putting any two pieces together. Get them to understand that they are hypothesis testing by grouping the pieces by whatever character that they are using (color, pattern, shape). Ask them why their hypotheses fail so often. Get them to understand the problem that science deals with when you make assumptions based in incomplete data. If they were able to take all the characteristics of each piece and make a perfect analysis they would never be wrong in their choice of which pieces fit where, but using the mark I eyeball and only a limited set of characters you often make mistakes. You have to expect to be wrong quite often in science. You have to be able to test your hypotheses.
A few students always assemble the edge of the puzzle first. I point out that this is just what scientists try and do when they create a framework and build on it. We usually get the easiest pieces in place first and the edges are the easiest pieces to fit because they only have three interacting sides to consider. Science does what it can and builds on it. About this time someone notices that I've taken away the corner pieces. When they ask for the corners I ask them how they know that the puzzle has corners. It isn't a trick question. We make assumptions like this all the time, and it is based on our experience, but they can also see that some pieces are missing based on their expected square side and only two interacting edges. They have a hypothesis that something is missing and it is based on their experience and the physical evidence. I throw out the corners and they have to scratch their heads because I've given them the corners to another puzzle, but they still fit and they still complete the outside of the puzzle. I tell them that science is full of pieces that don't quite fit, but that are good enough to help us get a better idea of what it is that we are working on.
As the puzzle gets completed I make them note how the qualitative as well as quantitative nature of the hypotheses that they are testing improves as they acquire more knowledge of what the picture looks like. The picture never gets perfect because the corners don't match, but it is obviously good enough to get a pretty good idea of what the picture is.
I don't think that I've ever brought up creationism or ID in this lecture, but if you want to you can just state the fact that ID as a "concept" has never been able to place a piece in the puzzle of nature. They have tested quite a few pieces to see if they fit, but there isn't a single one left in place at the end of the day. Essentially, it is a concept with a 100% failure rate upon testing. The only pieces left on the board are the ones that haven't been tested yet. It has been found to be worse than just randomly picking any two pieces and trying them to see if they fit. If any student doesn't believe this, just ask them for a single piece that ID has placed in our scientific knowledge. You won't find a list of these things at the Discovery Institute because there are no ID scientific successes. The farce is that they have lists of scientists that were or are religious and state their scientific successes without telling anyone that usually these guys were responsible for kicking out an ID piece from where it didn't belong. These guys are known for their scientific contributions and not their ID contributions. This is why many scientists define science in such a way that ID is excluded from consideration. It simply has never worked, and it has been a monumental waste of time. Definitions like those that exclude ID get put in place to protect the incompetent from themselves. Most rational scientists can figure out for themselves that they can think about ID, but they can't really expect to use it for anything. Not a single success and a 100% failure rate upon testing is pretty convincing to most scientists.
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Subject: Re: Protein Sequence Flexibility - Sean's evasions Date: 27 February 2005 Message-ID: email@example.com
>Evolution must proceed by randomly changing either
>single or multiple amino acid residues until it
>hits upon something that has improved beneficial
>function over what came before.
Not quite. Structural elements are what matters. That is how you can have proteins which are practically identical structure-wise, while having almost no sequence homology.
So what evolution has to "stumble on" is an overall fold. There aren't that many of them, only a few thousand. Functionality is then derived from modifications to those folds. But we covered this several times already. You listened, and then parroted your previous fallacious argument.
>If there is no detectable change in function with a
>change in sequence, nature is blind and cannot select
>between different sequences.
>This creates a neutral gap problem that is indeed
>completely random until something that is actually
>functionally selectable comes along - by pure chance
>or random walk.
Correct fact, incorrect interpretation.
A protein can have a function X. The same protein can be altered significantly - increased in size manyfold, for example, by an insertion - while keeping the function. Another fold can appear on the added sequence (or be transplanted from elsewhere), which retargets the protein; or even gives it another, vastly different function.
>The odds of happening upon a new selectable sequence
>are the same either way.
Which you determine exactly how? By assuming random walk through single residues. Right back to your strawman. Which, in fact, you again state here:
>At low levels of minimum sequence complexity (a few dozen
>or so fairly specified amino acid residues), evolution
>is quick and easy for all organisms because something in
>the genome will be only one or two residue changes away.
Minimum sequence complexity, again. A completely meaningless term which you invented to obfuscate the issue, and hide your strawman.
Here is some homework for you. Since you exibited extremely poor ability to search the literature in this post of yours (see below for details), let me see if you can do this (it has been done): how many completely random 350aa sequences do you need to form in order to come up with a fairly specific DNA-binding activity?
There is a reason why there are so few folds used in nature. Evolution stumbles on, say, a zinc finger (which it did repeatedly; it is very easy to create one of those). Then it modifies it for a sequence specificity that gives a selectable advantage. This process is vastly different than the one you propose.
Since I'm bored at the moment (buffer exchange; faster than dialysis, but requires you to babysit the centrifuge - the bloody bugger is precipitating in the membrane if I allow the gradient to get too steep), let me waste some more time and draw the difference out for you.
According to you, you have a protein. Then you have completely random changes to the protein, which you treat as single point-changes, which then lead to a new functionality. This is, as you correctly note, far too slow a process to account for variability we observe.
However, evolution does not work like that. What happens is that mutations transfer entire domains and stretches of sequence around; or random insertions form completely novel domains and folds. These changes can have 1) a negative effect (somewhat likely), in which case they are selected against; 2) neutral effect (most likely), in which case they will remain in the genome to be acted upon further; 3) positive effect (unlikely in the first iteration), in which case they are selected for.
The most frequent case, therefore, will be: protein has changed, there are all these disordered loops or extra helices, barrels, sheets, whatever - but it still works. Activity may be affected, but not sufficiently to make a large difference.
What happens then? Small mutations will affect these new domains and alter their specificities. Again, there is a reason why so much of the biochemistry follows similar paths and similar reactions. The protein folds are similar. Evolution relies on taking something that already exists, and altering it slightly, to produce a novel effect. The cumulative effect over a long period of time can be staggering - as directed evolution experiments have shown, and as observed evolution in the last century has shown.
And "cumulative" here isn't just mentioned in terms of adding things to the same sequence. Once a fold appears in the genome, it can be transplanted elsewhere, and you have a boom in the number of its uses all over the place.
>This has a stalling effect on evolutionary potential
>until evolution cannot proceed at all, this side of
>trillions of years of average time, beyond very low
>levels of functional complexity.
Right. Therefore, enteroccoci have always been resistant to vancomycin, right? The Designer designed their resistance at the dawn of time...
Or don't you know? Vancomycin resistance involves a radical change to the structure of cell wall, development of five different genes, all of which are required to act simultaneously in concert, in order to produce the resistance. I forget the total length, but we are talking a few thousand amino acids here, "acting together". With regulation, and differential expression.
Not that the number of amino acids, which you are so fixated on, has anything to do with complexity. The number and complexity of reactions is what actually matters.
Bacteria developed resistance to penicillin within a year of its introduction. As you acknowledge yourself, it is an easy resistance to develop. Development of resistance for vancomycin took 30 years, as it is so complex. It would have probably taken much longer, if it wasn't for use of avoparcin (a similar peptidoglycan antibiotic) as a feed additive of farm animals.
But still, 30 years, for something you say requires many trillions of years. Good work for enterocci, don't you think?
>Really, all the hot air you blew around last time you
>responded to this challenge isn't improved upon by
>this current post of yours.
Actually, the only one blowing hot air around here is you.
>Functional sequences just don't overlap anymore in a way
>that natural selection can walk across a bridge of improved
>function like it did at low levels.
They overlap almost completely. Which is why you don't have billions of folds, you have thousands. And only a few dozen are responsible for the vast majority of the truly important chemisty in the cell.
Still not clear enough? Take three proteins with vastly different functions. Let's pick three:
In your model, evolution has to start with one protein, then random-walk until it gets a sequence that is "specific" for the new function.
In reality, all of the three above are based around a beta-roll domain. The domain develops. Once the domain develops, additional mutations confer various different functions to it. Add a generally hydrophobic helix to one side, and you have made it into a membrane protein. Add a few hydrophylic loops, and there you have it swimming in the cytosol. Change a glycine into a histidine, and look there, it binds zinc, and performs a completely different chemistry.
Take a look at the CATH database. Go through the various protein classes. See how similar they are? It's all about structure/function, Sean.
>completely random evolution just can't do much
>this side of trillions of years of time.
And yet it does, as so many examples show.
Add development of resistance to cancer-treating drugs by cancer cells to the growing list we have here. You won't look at it, of course, but others might want to check it out for more arguments to clobber you with next time you rear your head. Some very different functions, and yet oh so close to each other as to be readily reachable by mutations within a few years in the life of a cancer patient.
>Yes, you can - but will you ever come across anything
>new beyond low levels? I don't care about the original
>function at all. I only care about how evolution comes
>up with new types of functions beyond very low levels
>of complexity (i.e., greater than 1000 codons at minimum)
Number of codons, again, has nothing to do with it. It is much more difficult to evolve two steps in a reaction, each involving a 100aa protein, then a single protein that performs a single reaction, yet is 1000aa long. Again, structure/function.
>Yes, they are many, but none of them help you. The odds
>of correct sequence formation is the same as it is with
>single point mutational changes.
Not true. You don't seek the "correct" structure. You seek a general fold. Once that fold has a very minor activity that is desired by the cell, it gets funneled into improving very quickly (as you did concede yourself in our previous discussion). The exact sequence of amino acids is completely irrelevant, as long as the fold performs the chemistry you want.
>They could easily come together to make a 1000
>codon function - right? No.
Since you repeat yourself (as if repetition will make your statements more true), I'll do the same.
One, 1000 codon function is a meaningless term. Two, they did. I've given you examples. You ignored them. I've given you a few more just now. You'll ignore them too.
>Huge problem - right?
>Neither one of these proteins requires over a few
>hundred fairly specified amino acids at minimum.
>(DNA ligase III requires < 200aa for function and
>PARP 1 requires < 700aa) What is your point then?
Here is the aforementioned poor research.
DNA ligase III is a 920+ residue protein, PARP is well over 1000. If that is still too uncomplicated for you, there is the vancomycin resistance mentioned above. Or we can go back to pterin biosynthesis pathway (which you neatly skipped the last time). Or back to lactase, or are you willing to concede there that it is not irreducibly complex?
>Not until you actually bring something relevant to the table . . .
I've asked you many times, you still won't answer:
What would you consider relevant? What kind of evidence would be sufficient to prove to you that you are wrong?
Is there any?
I'm frightened by your ignorance of biochemistry, considering that people actually come to you for treatment. I'm also saddened by the fact that only those of us who are pretty well-versed in it can recognize your crap, and that you will manage to fool a lot of people into believing you. However, it is the basis of your reasoning that wearies me the most. I've read your opinion here:
...and it states the reasons you keep distorting science quite well. The thoughts of a True Believer are so direct and obvious that it is no wonder you are unable to accept evidence contrary to your position. You have tied your God to some very silly notions, and now you have to protect them, or your God will sink along with them. This is not the fault of God. It is your own fault. Science isn't wrong. Scripture doesn't have to be wrong. What is wrong is your interpretation of the scripture.
I'm digressing. Why am I talking about this at all?
Unlike you, Sean, I don't know if there is a God. However, I can imagine a God. I can look around myself, put together everything I know about the universe, and say: "If there is a God, these are the properties that God would have to have". Among those properties is the fact that he was able to create a small set of incredibly elegant basic laws, organize matter and energy according to them, and let the Universe go.
And you had the Big Bang, and you had the formation of the vastness of spacetime. And you had the spark of life, and then evolution which led to the marvel of the human mind. And it is a beautiful picture. From initial light, over lives and deaths of stars, to us: wondering where we fit in the great picture. Living starstuff, energy of the sun coursing through our veins, staring at the darkness and thinking about the Creator.
Then you come to me, and tell me: "No. That cannot be true. God is a magician. He created the laws of the universe, just so he could promptly break them by performing miracles. That picture scientists have reconstructed is nonsense. God put together some powdered rock, uttered a word or waved his magic wand, or something, and there, poof, in a cloud of smoke, was Adam, fully formed. That is the way it happened, and if you claim anything different, you are an enemy of God, and you are trying to destroy him!"
If there is anyone here who blasphemes, it is you and your creationist ilk. The fact that you continue to pile lie upon an untruth upon a distortion of facts, all in order to "defend" God from "evilutionists" is just an added blasphemy added to the long list.
And if He indeed does exist...oh, to be a fly upon the wall when you finally meet Him...
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