Sunday, June 26, 2011

The Vision Cascade is Initiated Not by Isomerization but by Force Field Dynamics

As you read these words a frenzy of activity is taking place as the light entering your eye triggers a highly detailed sequence of actions, ultimately causing a signal to be sent to your brain. In fact, even a mere single photon can be detected in your vision system. It all starts with a photon interacting with a light-sensitive chromophore molecule known as retinal. The interaction alters the retinal molecule and this, in turn, influences the large, trans-membrane opsin protein to which the chromophore is attached. This is just the beginning of the cellular signal transduction cascade. In the next step the opsin causes the activation of hundreds of transducin molecules. These, in turn, cause the activation of cGMP phosphodiesterase (by removing its inhibitory subunit), an enzyme that degrades the cyclic nucleotide, cGMP.

A single photon can result in the activation of hundreds of transducins, leading to the degradation of hundreds of thousands of cGMP molecules. cGMP molecules serve to open non selective ion channels in the membrane, so reduction in cGMP concentration serves to close these channels. This means that millions of sodium ions per second are shut out of the cell, causing a voltage change across the membrane. This hyperpolarization of the cell membrane causes a reduction in the release of neurotransmitter, the chemical that interacts with the nearby nerve cell, in the synaptic region of the cell. This reduction in neurotransmitter release ultimately causes an action potential to arise in the nerve cell.

New research is now helping to explain the details of the first step in this Rube Goldberg machine. What happens when the photon interacts with the retinal molecule? And how does this influence the opsin protein? It had been thought that the key step was a change in the structural configuration of the chromophore. This photoisomerization is caused by the photon and was thought to be how the chromophore influences the opsin.

The new research, however, found that when isomerization is disabled the vision cascade continues to function normally. It seems that a key step, occurring before isomerization, is a shift in the electron distribution of the chromophore. This shift modifies the electric field surrounding the molecule, and this in turn influences several amino acids of the opsin protein, which in turn leads to the activation of the transducin molecules.

An argument from ignorance?

As is typical these new findings do not bode well for evolution. Think of it, evolution designing force fields. But evolutionists cry foul. “You are arguing,” they say, “that since you can’t imagine how evolution could have created such a design that evolution therefore is false. That is nothing more than an argument from ignorance.”

You will be told you don’t understand how science really works and that such findings don’t harm evolution at all. In fact, they open new avenues for understanding how evolution works. Far from a problem for evolution, they enlarge our understanding of what has long since been known to be a fact.

A big design space

Well is it fallacious to think such findings are problematic for evolution? A key issue is the design space. Imagine that a mutation occurs somewhere in a segment of DNA. And imagine that a particular residue within that DNA segment needs to be a certain base, say cytosine. There are a total of four possible bases (adenine, guanine, thymine and cytosine). So the design space for that residue has a total of four possible choices, and the needed design constitutes 25% (one in four) of the design space. It won’t require too many mutations to luckily obtain the needed cytosine. In this case evolution seems reasonable.

But real-world, biological designs require a great deal more than the specification of a single DNA residue. Proteins, for instance, require a great many DNA residues to be specified. Even a single, typical protein requires more than 10^100 (a one followed by one hundred zeros) evolutionary experiments to find. This is an astronomical problem that is well beyond evolution’s capabilities. See here, here, here and here for more details.

In other words, for a typical protein the design space is large and the number of selections, within that design space that work, is relatively small. Instead of a 25% chance of success as we saw in the above simple example, it is many many billions and billions of times less likely. Even optimistic estimates of how many evolutionary experiments are possible fall many orders of magnitude short of what is needed to evolve a protein. Evolutionary theory simply doesn’t work.

Does evolution shape force fields?

The new research presents a different problem for evolution. In addition to designing the opsin protein, evolution must now design the electric field surrounding the chromophore, and how it responds to photon interaction. And while it is busy with that task, it must also specify the correct amino acids at the correct locations within the opsin, that will be influenced by the chromophore’s dynamic electric field.

This massive design problem involves what is known as an n-body solution. That is, the various sub atomic particles in the opsin amino acids and the chromophore, including the chromophore’s flowing electrons which respond to the photon, all contribute to the environmental force fields.

Modeling these force fields and how molecules respond to them is a major problem in molecular dynamics studies. Both the modeling of the force fields, and the molecular dynamics is challenging and computationally intensive. For instance, each particle influences each of the other particles. And as a particle moves, all of its influences change. But other particles are moving as well, so the dynamics quickly become extremely complicated.

The previous model, which had evolution designing the chromophore and its photoisomerization, was complicated enough. Now evolution must also design force fields and their dynamics caused by electron flow within the chromophore. The design space just took another quantum leap.

An argument from ignorance or theory protectionism?

Needless to say evolutionists have only the usual hand-waving speculation to explain the evolution of such designs. The problem is not that skeptics cannot explain how evolution can create such designs, the problem is that evolutionists cannot explain it. Skepticism of evolution is not a consequence of ignorance, it is a consequence of the theory falling far short of its claims. The fact is evolutionary theory doesn’t work and evolutionary cover-ups are nothing more than theory protectionism. Religion drives science and it matters.

10 comments:

  1. The eye is an incredibly elegant and efficent design. As King David said 3000 years ago, we are wonderfully made. Evolutionist find themselves again on the short end of the stick.

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  2. Thanks again Cornelius for yet another very informative post. Truly, I find more science here than anything PT or other so-called science blogs put up.

    Force and information are at the heart of life's processes, and the fact that both are immaterial makes it all that more fascinating. Mind without doubt is our last and great frontier of exploration.

    Keep up the fantastic job.

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  3. Hunter: Even a single, typical protein requires more than 10^100 (a one followed by one hundred zeros) evolutionary experiments to find. This is an astronomical problem that is well beyond evolution’s capabilities.

    Cornelius,

    It would be an impossibility if evolution (a) were searching for one specific protein and (b) did so via a random search. Neither of these is correct.

    You keep making this mistake as if no one has ever corrected you. Can you ever learn?

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  4. Here is one such correction from Joe Felsenstein. Your reaction shows that you are aware of this criticism. Yet you keep using the same misleading argument.

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  5. "In fact, even a mere single photon can be detected in your vision system."

    While I heard this before (I think by Simon Conway Morris) this sentence demonstrates a lack of understanding of pretty basic physics. The light-sensitive chromophore molecule necessarily detects one single photon.

    Such a mistake would be forgivable if it was not made by someone thinks that on the basis of such an understanding he could judge the validity of entire theories.

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  6. Just finished reading article.

    Wow , I had no idea light sensing worked like that. We are talking nano-scale tuned photon transducer-amplifier.

    I want one of those !!!

    Oh, wait – I have two already.

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  7. second opinion: ...this sentence demonstrates a lack of understanding of pretty basic physics. The light-sensitive chromophore molecule necessarily detects one single photon. Such a mistake ....

    Where's the mistake? So the PhD physicist behind the blog states in passing a detail obvious to other scientists and you call this a mistake? Excuse me, but I knew not much about the cascade from a single photon that can give rise to an action potential. And our host is bringing recently determined information on how electric potentials are designed into a crucial mechanism in this cascade. Would you care to venture a guess as to HOW MANY random mutations it took to give rise the the mechanism at the focus of this post, the utilization of electric fields at the stage described? In other words, something constructive to the debate instead of this huffa puffa indignation apparent in your reply.

    ... he could judge the validity of entire theories.

    Well -- as if billions of people haven't already done so, and without your approval, boo hoo. The arrogance of it!

    When you guys can give no details on how any complex structure arose by RMNS you find yourself the butt of jokes by the educated and non-educated alike. And so the majority in this country and in most others don't believe you guys with your polemic-driven agenda.

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  8. oleg: Yet you keep using the same misleading argument.

    so given monkeys typing billions of trillions of characters, you assume there can be no one watching, named Natural Selector, who could be on the lookout for a great play? What a goofy argument.

    The onus is on you guys to even begin to admit the sheer astronomical numbers of mutations required to generate the spectacular biochemical and physical chain of events described in this thread, before the function could even be selected as a benefit to survival.

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  9. Since we're talking proteins and probabilities...

    Given a protein with function, it is still astronomically improbable (it would take > 10^15 Gyrs) that that protein would mutate into a homologous structure with different function.  And this should have happened over 1,000 in evolutionary history.  See links below.  How do Darwinists respond to this data?

    http://biologicinstitute.org/2011/04/16/when-theory-and-experiment-collide/

    http://bio-complexity.org/ojs/index.php/main/article/view/41

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  10. rpvicars: http://bio-complexity.org/ojs/index.php/main/article/view/41

    IDers try to evolve a cat into a dog and fail, therefore Design!

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