Cell Trends

[bob b]

And the sum total of the proof you have offered under direct questions – is for you to (once again) run like a scared jackrabbit from the simple math. Aerospace systems engineer? Hah, bad, really bad joke. I gave you the specific scenario to address the claim. You are the one who is too cowardly (or incompetent) to give answer to it.

So now the status of the creationist claims in his OP – 1) Childish silliness in portraying molecules a brainless and blind, and 2) Broad claims about the viability of cells that didn’t have protein repair mechanisms, claims that the bob b can’t defend without adding new conditions to, an then resorts to his oft-used tactic of ignoring everything that was said that he can’t handle.

Maybe we should go back to vectors and Joshua’s long day. Bob b has had a year or so to learn what vectors are, maybe he can defend that thread now.

Why is it that Bob b is primarily active in commenting on evolution - a field in which he has no technical or educational experience, and even there he limits himself to the safety of “Nobody in their right mind would believe that” type generalities? I just wish he would wander more often into the world of astronomy and physics. I need to play with him too.

Apparently ThePhy can only criticize what others say, but runs like a scared rabbit when asked to present support for his own claim that cells do not really need a correction mechanism.

"I claim it is perfectly possible for many types of cells to multiply sans such a mechanism".

 

[ThePhy]

Apparently ThePhy can only criticize what others say, but runs like a scared rabbit when asked to present support for his own claim that cells do not really need a correction mechanism.

I have presented an explicit simple mathematical example that you are mightily ignoring. So this stands as not only another example of your fundamental incompetence at elementary mathematics, but now as a classic demonstration of your willingness to blatantly lie. Your are below being either a mediocre scientist or a mediocre Christian.

 

[Stripe]

I have presented an explicit simple mathematical example tha....

long division...?

*hopelessly overeager pandering*

 

[bob b]

How Life Defends Against Harmful Mutations 01/31/2002
Different populations have different ways of defending themselves against the destructive effects of harmful mutations, say David C. Krakauer of the Sante Fe Institute and Joshua B. Plotkin of Princeton, in a paper “Redundancy, antiredundancy, and the robustness of genomes” in the Jan 29 Proceedings of the National Academy of Sciences. Although presuming genetic mutations are a source of evolutionary novelty, they explain that damage must be guarded against.

The authors propose that small populations of large organisms (like mammals) use redundancy to maintain fitness: i.e., copies of genes and backup systems. But large populations of small organisms, like bacteria, appear to employ antiredundancy strategies: i.e., they are hypersensitive to mutation, but employ methods of removing harmful mutants:

“Assuming a cost of redundancy, we find that large populations will evolve antiredundant mechanisms for removing mutants and thereby bolster the robustness of wild-type genomes; whereas small populations will evolve redundancy to ensure that all individuals have a high chance of survival. We propose that antiredundancy is as important for developmental robustness as redundancy, and is an essential mechanism for ensuring tissue-level stability in complex multicellular organisms. We suggest that antiredundancy deserves greater attention in relation to cancer, mitochondrial disease, and virus infection.”

The authors propose a mathematical model for explaining the dynamics of redundancy and antiredundancy in differing populations. Populations exhibiting redundancy have hilly fitness landscapes with steep, narrow peaks. Antiredundant populations have a flat fitness landscape with small peaks, forming a “quasispecies” of mutants with similar fitness.

Although this paper is listed in the category “Evolution,” it is hard to see how it helps evolutionary theory. Whether a population is large or small, it works to shield itself from mutations and achieve stability. The fitness peak concept comes from graphing fitness as the vertical axis on a 3D plot of a population. Evolutionists have been realizing that fitness is not a progressive slope of “onward and upward” improvement, but an undulating landscape with peaks and valleys. A population on a peak is stable, and would actually have to devolve to get off its peak and onto a higher one. This is not evolution in the Darwinian sense. It fits in better with the view that natural selection is a conservative process, allowing enough variation to compensate for contingencies (like mutations) that would otherwise destroy the population. The authors do not describe how “evolutionary novelty” can become established, nor do they provide any example of a beneficial mutation. It appears, therefore, that this paper is promoting a view of life being in a state of dynamic equilibrium, not upward evolution.

 

[Johnny]

The eject button is on your left.

 

[bob b]

DNA Damage Response Team to the Rescue 01/04/2002
Americans proudly hail the firefighters and cops that go to work when terror strikes, but did you know your body has an even more heroic team that flies into action when DNA gets damaged? It’s called the DDR - DNA Damage Response team. The hearty band of specialized enzymes can handle any contingency: broken strands, loose ends, typos, kinks, twists and numerous other emergencies. During complex operations like duplication and translation, the DDR team has its P&P (policies and procedures) down pat, including checkpoints and feedback mechanisms to ensure repairs are made quickly, or that irreparable damage triggers the appropriate salvage and disposal operations.

Writing in the Jan 4 issue of Science, a team of seven geneticists, biochemists and biologists have determined that no less than 23 separate genes code for the DDR (and there are probably more). In addition, they noted an “extraordinary level of conservation of molecular mechanisms in DDR pathways” in all living things, from the worms they studied to man. Many kinds of cancer can be traced to defects or mutations in these genes, that leave the cell like a city without a fire department.

 

[aharvey]

How Life Defends Against Harmful Mutations 01/31/2002
Different populations have different ways of defending themselves against the destructive effects of harmful mutations, say David C. Krakauer of the Sante Fe Institute and Joshua B. Plotkin of Princeton, in a paper “Redundancy, antiredundancy, and the robustness of genomes” in the Jan 29 Proceedings of the National Academy of Sciences. Although presuming genetic mutations are a source of evolutionary novelty, they explain that damage must be guarded against.

The authors propose that small populations of large organisms (like mammals) use redundancy to maintain fitness: i.e., copies of genes and backup systems. But large populations of small organisms, like bacteria, appear to employ antiredundancy strategies: i.e., they are hypersensitive to mutation, but employ methods of removing harmful mutants:

“Assuming a cost of redundancy, we find that large populations will evolve antiredundant mechanisms for removing mutants and thereby bolster the robustness of wild-type genomes; whereas small populations will evolve redundancy to ensure that all individuals have a high chance of survival. We propose that antiredundancy is as important for developmental robustness as redundancy, and is an essential mechanism for ensuring tissue-level stability in complex multicellular organisms. We suggest that antiredundancy deserves greater attention in relation to cancer, mitochondrial disease, and virus infection.”

The authors propose a mathematical model for explaining the dynamics of redundancy and antiredundancy in differing populations. Populations exhibiting redundancy have hilly fitness landscapes with steep, narrow peaks. Antiredundant populations have a flat fitness landscape with small peaks, forming a “quasispecies” of mutants with similar fitness.

Although this paper is listed in the category “Evolution,” it is hard to see how it helps evolutionary theory. Whether a population is large or small, it works to shield itself from mutations and achieve stability. The fitness peak concept comes from graphing fitness as the vertical axis on a 3D plot of a population. Evolutionists have been realizing [ever hear of Sewell Wright?] that fitness is not a progressive slope of “onward and upward” improvement [this is written as if creationists have understood that fitness is not a measure of progress and improvement! ], but an undulating landscape with peaks and valleys. A population on a peak is stable, and would actually have to devolve to get off its peak and onto a higher one. This is not evolution in the Darwinian sense [Okay, so I guess you haven't ever heard of Sewell Wright!] . It fits in better with the view that natural selection is a conservative process, allowing enough variation to compensate for contingencies (like mutations) that would otherwise destroy the population. The authors do not describe how “evolutionary novelty” can become established, nor do they provide any example of a beneficial mutation. It appears, therefore, that this paper is promoting a view of life being in a state of dynamic equilibrium, not upward evolution.

News flash: Creationsafaris foils another attempt to foist "piece of the puzzle" fallacy onto unsuspecting public!

Yet another experiment that doesn't explain it all: when will they learn?​

 

[aharvey]

DNA Damage Response Team to the Rescue 01/04/2002
Americans proudly hail the firefighters and cops that go to work when terror strikes, but did you know your body has an even more heroic team that flies into action when DNA gets damaged? It’s called the DDR - DNA Damage Response team. The hearty band of specialized enzymes can handle any contingency: broken strands, loose ends, typos, kinks, twists and numerous other emergencies. During complex operations like duplication and translation, the DDR team has its P&P (policies and procedures) down pat, including checkpoints and feedback mechanisms to ensure repairs are made quickly, or that irreparable damage triggers the appropriate salvage and disposal operations.

Writing in the Jan 4 issue of Science, a team of seven geneticists, biochemists and biologists have determined that no less than 23 separate genes code for the DDR (and there are probably more). In addition, they noted an “extraordinary level of conservation of molecular mechanisms in DDR pathways” in all living things, from the worms they studied to man. Many kinds of cancer can be traced to defects or mutations in these genes, that leave the cell like a city without a fire department.

As creationsafaris themselves put it, "Did you catch the personification fallacy there?" No? You might need to step back a bit; creationsafaris practically saturates their writing with personification, the better to create the illusion of intelligence (and therefore design) in their systems.

 

[Johnny]

I'd be embarassed if that were my resource.

 

[bob b]

Ancient Cells Proofread Better 01/08/2002
Four biochemists from Stratagene in California, writing in the Proceedings of the National Academy of Sciences, have identified a complex “proofreading” enzyme that improves DNA copying accuracy up to 100-fold. The enzyme is composed of multiple protein chains and can survive high temperatures (around 200oF). Although with this proofreading enzyme copying is slowed down (550 nucleotides per minute instead of 2,800 without the proofreading), the fidelity is greatly increased. It apparently works by breaking down a product called dUTP produced by other construction pathways. dUTP can poison a replicating DNA chain by substituting uracil. All living things contain a suite of proofreading enzymes, including members of this family of enzymes (dUTPases) that “read ahead” and find dUTP to cut it out of the growing DNA strand. But this one is not only highly effective, it works at high temperatures. The surprise is that this bulky, complex enzyme was found in a single-celled organism of the kingdom Archaea (“ancient ones”) which includes bacteria that thrive in hot springs.

This paper demonstrates that it is a serious injustice to label one-celled organisms primitive. They may be small and unicellular, but they are not primitive. In fact, they appear to have superior engineering in many ways (notice that this enzyme works a lot faster than a human typist!). Astrobiologists frequently talk about extremophiles (organisms that can tolerate extreme environments like hot springs, high salt, cold Antarctic ice and deep sea vents), as if they demonstrate that life is easy to evolve on other planets. Their name Archaea imply that they are ancient, primitive organisms. A better paradigm is to view these organisms as over-engineered so that they can adapt to special situations, similar to how a race car engine, designed to “push the envelope” at higher speeds and temperatures, is superior to your sedan.

Just think for a moment about the amazing fact (discovered in our lifetime) that living things have editors and proofreaders! Many word processors today include automatic spell checkers; would anyone believe for a moment that Microsoft Word XP was a result of impersonal trial and error? Now that we observe superior hardware and software engineering in the living cell, the time is come for scientists to abandon their allegiance to the untenable philosophy of naturalism, and face the music: intelligence is an indispensable causative factor in the life sciences.

Note: Several other papers on DNA proofreading can be found in the January 8 preprints of PNAS, each equally interesting and amazing, such as this paper by biochemists at the University of Washington on nucleotide excision repair (NER), the ability of enzymes to repair breaks in DNA caused by ultraviolet light damage. (They studied this in yeast; how did yeast hire linemen?)

 

[SUTG]

Q Professor Behe, right before the break you said
that the findings accumulated over 140 years that support
the contention that Darwinian processes could explain
complex molecular systems total a number of zero, correct?

A I ll -- I think I did, yes.

Q Okay. And that s a proposition you stand by.

A Well, again, you have to look at the papers. And what I meant by that is ones which fully explain how random mutation and natural selection could build a complex system; yes, there are no such explanations.

Q Zero papers.

A I don t think I said zero papers, perhaps I did, but there are zero explanations.

Q And zero is the same number of articles in peer-reviewed scientific journals that argue for the intelligent design of complex molecular systems?

A The number of peer-reviewed papers in scientific journals which show that life is composed of molecular machinery that exhibits the purposeful arrangement of parts in detail on term, you know, many many many thousands. There are -- I think there are just one or two that mention intelligent design by name.

Q That argue for the intelligent design of complex molecular systems in peer-reviewed scientific journals?

A No, I don t think -- now that you mention it, I think that I was thinking of something else.

:rotfl: source.

 

[SUTG]

Q But you are clear, under your definition, the definition that sweeps in intelligent design, astrology is also a scientific theory, correct?

A Yes, that s correct..

 

[bob b]

Introns Found in Primitive Eukaryote 02/26/2002
Another evolutionary assumption needs revision. Science Now reports that introns have been found in Giardia, a primitive eukaryotic single-celled organism. Sometimes considered “junk DNA,” introns are pieces of genetic code that do not code for proteins, that have to be cut out of the strand by genetic scissors called spliceosomes before transcription can begin. Introns were thought to have evolved later in the eukaryotic line, but here they were, scissors and all, in an early “primitive” eukaryote. The original paper is in the Feb 19 Proceedings of the National Academy of Sciences.

Introns are a bit of a mystery as to their function, but we have learned to question the assumption that anything in biology is useless. The machinery to handle introns and move pieces of genetic code around is very sophisticated and complex. Introns and transposons are subjects of intense research; indications are that they will prove to be vital for proper operation of the cell. This story puts more pressure on evolutionists to explain how complex machinery that cuts and splices DNA – and knows just where to put it – could have evolved by chance in the earliest, simplest nucleated cells.

 

[SUTG]

ROTHSCHILD: [...]Your argument is that,
even if the type III secretory system is a pre-cursor to
the bacterial flagellum, is a subset, the bacterial
flagellum is still irreducibly complex because that
subset does not function as a flagellum?
BEHE:. That's correct, yes.
Q. And, therefore, the bacterial flagellum must have
been intelligently designed?
A. Well, again, the argument is that, there is --
that when you see a purposeful arrangement of parts,
that bespeaks design, so, yes.
Q. And yesterday, you testified that, that doesn't
mean the bacterial flagellum was necessarily designed,
appeared abruptly in one fell swoop, correct?
A. That's correct.
Q. Could have been designed slowly?
A. That's correct.
Q. So under this scenario, at some period of time,
the bacterial flagellum wouldn't have had all of its
parts until the design was completed?
A. Could you say that one more time?
Q. Yeah. Under this scenario of slow design --
which was what I experienced with my kitchen -- at some
period of time, the bacterial flagellum wouldn't have
had all its parts until the design was completed?
A. That's right.
Q. And so without all its parts, it wouldn't be
functional?
A. That's right. Not as a flagellum, yes.
Q. So that is a phenomenon in both intelligent
design and natural selection?
A. I'm not quite sure what you mean.
Q. In slow design, the bacterial flagellum has some
prior existence, it doesn't have all its parts, right?
A. Well, if -- until it has all its parts and it
starts functioning, I guess it's problematic to call it
a flagellum.
Q. It has some subset?
A. I guess things that will eventually be part of
the flagellum would begin to appear, yes.
Q. Just not function like a flagellum?
A. Yes, the system would not yet function as a
flagellum.
Q. Just like has been suggested for natural
selection?
A. I'm sorry.
Q. Just like has been suggested for natural
selection?
A. I'm not quite sure what you mean.

 

[aharvey]

"You must spread some reputation around before giving it to SUTG again." Sorry about that, dude, but keep up the good work! Even if it means I can't unsubscribe to this otherwise intellectually bankrupt thread!

 

[mighty_duck]

This story puts more pressure on evolutionists to explain how complex machinery that cuts and splices DNA – and knows just where to put it – could have evolved by chance in the earliest, simplest nucleated cells.

So, there are redundant pieces of DNA, and functions that remove this redundancy. You can't think of a way for those two to have evolved together? Even personal incredulity has its limits!

And calling a modern-day cell "primitive" seems to imply that the first cell must have been similar to that. It is a false implication.

 

[bob b]

Bewildering Complexity – RNA Editing 02/21/2002
The Feb 22 issue of Cell contains a paper by Alabama biochemist Stephen J. Hajduk entitled “Editing Machines: The Complexities of Trypanosome RNA Editing.” RNA editing is critical to the accurate building of molecular machines like ATP synthase vital to cells. The author asks, “How many proteins does it take to edit an RNA?”

"Recent studies, using conventional protein purification, homology modeling, and mass spectrometric analysis, have focused on identifying the components of editing complexes. This is an important yet somewhat bewildering exercise since at least a dozen proteins have been identified that putatively contribute to RNA editing in trypanosomes."

He describes how these proteins form editing complexes, and how RNA strands pass through several iterations of editors on their way to the protein assembly plant. In the last section, “Increasing complexities and unresolved issues,“ Hajduk states: “As we begin to understand the composition of the editing machinery, new complexities emerge.”

The author does not explain how evolution could have built this machinery. He only notes that the machinery is “conserved” (i.e., unchanged in many types of organisms), suggesting that they had a common ancestor. Clearly, however, he is bewildered by the complexity of the system. There is no need to stuff the facts into an evolutionary box far too small for them. Simply describe them and let people think.

Creationists, too, need to think about these issues. This level of complexity is found in trypanosomes, which cause serious blood diseases, including sleeping sickness. This fact is part of the larger question of why there is disease, suffering and death in the world today. Many organisms responsible for disease and suffering show exquisite design. Evolution explains everything as competition for survival. But why would a trypanosome care whether it survives or not? And how could such high levels of organization, involving multiple interrelated parts (editing complexes; think about it), arise without design? On the other hand, if everything was designed, did the designer intend for the suffering? Intelligent design is sound science but incomplete philosophy; it needs an answer to suffering.

We mortals may not understand all the reasons, but Biblical creationism has a coherent answer. It describes a world that was created perfect, but was cursed temporarily because of sin. A sovereign Creator has the right to punish and judge disobedience. The Bible clearly teaches God does so; God makes no apology for sending pestilence, disaster, and plague according to His own will, though it grieves Him, and He desires all people to repent and be saved. The original curse could have involved modification of existing structures to become agents of harm, as a constant reminder of the consequences of sin and the imminence of death. Yet the Bible also makes clear that God did not leave Himself without witness, showing ample proof of His goodness (Acts 14). What better proof than to send his only Son to take the penalty we deserve? The mixed message of creation – beauty and suffering – is deciphered in Christ. You can be reconciled with your Creator at the foot of the cross.

 

[SUTG]

Q. You would agree that methodological naturalism has worked well for science?

A. Yes.

Q. And you would agree that it's largely responsible for most of the scientific progress we've seen?

A. No.

Q. If you could turn to Page 175 of your deposition. I'm going to read your answer there starting on Line 23. You say, I'm not doubting that methodological naturalism has worked for science and that it's largely responsible for lots of science that we've got, maybe even most of that we've got. Did I read that correctly?

A. Yes. I said maybe.

 

[bob b]

Protein Folding an Olympic Event 02/27/2002
A news release from the University of Pennsylvania puts biological molecules into the Winter Olympics:

"It’s a long-simmering debate in the world of physical chemistry: Does the folding of proteins into biologically active shapes better resemble a luge run - fast, linear and predictable - or the more freeform trajectories of a ski slope? New research from the University of Pennsylvania offers the strongest evidence yet that proteins shimmy into their characteristic shapes not via a single, unyielding route but by paths as individualistic as those followed by skiers coursing from a mountain summit down to the base lodge."

The researchers, who published in this week’s Proceedings of the National Academy of Sciences, found a great deal of variety in the paths and rates of folding. Only when a protein is folded correctly can it perform its function. Misfolded proteins are the cause of many serious diseases. The team explains that there are chaperones on hand to fix errors:

In the skiing analogy, chaperones could be thought of as rescue helicopters that return wayward skiers to the summit so they can try to make their way down the mountain again,” said [Feng] Gai, an assistant professor of chemistry at Penn.

Protein folding is fiendishly intricate, yet crucial to the chemistry of life - so much so that a small army of biologists and chemists has devoted itself to better understanding the process.

Another article in another source describes just how fiendishly intricate the process is. The March 12 issue of PC Magazine has a feature section on Technology in America. Alan Cohen describes how supercomputers, after showing their skill in deciphering the human genome, are trying to tackle the puzzle of protein folding:

"Problems like protein folding, where the number of possible shapes for the average-size protein is greater than the number of atoms in the universe, are far more complex. Thus, such problems require “a tighter, faster, parallel machine, where the processors of each work in conjunction with the others,” says Professor [David A.] Bader [director of the High Performance Computer Lab at the University of New Mexico]."

"... Advances like these require intense computation, and as impressive as the clusters that sequenced the genome are, they’re not enough for this new phase.
IBM’s Blue Gene project, which will be able to perform 1 quadrillion operations per second, sets out to tackle protein folding. IBM scientists estimate that calculating the folding process of even a very small protein on today’s most powerful computer would take 300 years. Even Blue Gene, once completed in 2005, will take a year to crunch the numbers."

In other words, the cell accomplishes with ease, thousands of times a day, within milliseconds, what today’s most powerful computers would take 300 years to figure out.
Proteins are likely to overshadow DNA as the hottest topic in biology. Most lay people think of meat or poultry when they hear the word protein, thinking of one of the basic ingredients of food, which of course, protein is. But on the molecular level, proteins are a toolkit of staggering complexity and design. Made up of chains of amino acids, all left-handed and often hundreds of units long, their precise folded shapes allow them to perform thousands of tasks in the cell. They are the Legos of molecular biology, but not just toy tanks and planes and soldiers, but real ones made of the same 20 building blocks.
Proteins shuttle cargo around, they speed up chemical reactions, they open and close gates into the cell and the nucleus, they form structural scaffolds and roadways, they proofread DNA, and much more. Perhaps most astonishing, they form actual motors that can spin up to 100,000 RPM (in the case of the bacterial flagellum). Modern biochemistry is pulling back the curtain on a new universe of microminiature machines that keep us, and the simplest bacteria, alive. In Darwin’s day, such wonders could not have been imagined. The time has come to cast off a paradigm far too simplistic to account for a technology this advanced.

 

[SUTG]

Q Back to my original question. What is the mechanism that intelligent design proposes?

A And I wonder, could -- am I permitted to know what I replied to your question the first time?

Q I don't think I got a reply, so I'm asking you, you ve made this claim here, "Intelligent design theory focuses exclusively on the proposed mechanism of how complex biological structures arose." And I want to know what is the mechanism that intelligent design proposes for how complex biological structures arose?

A Again, it does not propose a mechanism in the sense of a step-by-step description of how those structures arose. But it can infer that in the mechanism, in the process by which these structures arose, an intelligent cause was involved.

Q But it does not propose an actual mechanism?

A Again, the word "mechanism" -- the word "mechanism" can be used broadly, but no, I would not say that there was a mechanism. I would say we have an aspect of the history of the structure.

Q So when you wrote in your report that "Intelligent design theory focuses exclusively on the proposed mechanism," you actually meant to say intelligent design says nothing about the mechanism of how complex biological structures arose.

A No, I certainly didn't mean to say that. I meant to say what I said in response to that last question, that while we don't know a step-by-step description of how something arose, nonetheless we can infer some very important facts about what was involved in the process, namely, that intelligence was involved in the process.

:rotfl: