Tag Archives: Protein

What is intelligent design? Dr. Stephen C. Meyer explains the theory

A MUST-SEE lecture based on Dr. Stephen C. Meyer’s book “Signature in the Cell“. (H/T Chris S.)

You can get an MP3 of the lecture here. (30 MB)

I highly recommend watching the lecture, and looking at the slides. The quality of the video and the content is first class. There is some Q&A (9 minutes) at the end of the lecture.

Topics:

  • intelligent design is concerned with measuring the information-creating capabilities of natural forces like mutation and selection
  • Darwinists think that random mutations and natural selection can explain the origin and diversification of living systems
  • Darwinian mechanisms are capable of explaining small-scale adaptive changes within types of organisms
  • but there is skepticism, even among naturalists, that Darwinian mechanisms can explain the origin of animal designs
  • even if you concede that Darwinism can account for all of the basic animal body plans, there is still the problem of life’s origin
  • can Darwinian mechanisms explain the origin of the first life? Is there a good naturalistic hypothesis to explain it?
  • there are at least two places in the history of life where new information is needed: origin of life, and Cambrian explosion
  • overview of the structure of DNA and protein synthesis (he has helpful pictures and he uses the snap lock blocks, too)
  • the DNA molecule is composed of a sequence of proteins, and the sequence is carefully selected to have biological function
  • meaningful sequences of things like computer code, English sentences, etc. require an adequate cause
  • it is very hard to arrive at a meaningful sequence of a non-trivial length by randomly picking symbols/letters
  • although any random sequence of letters is improbable, the vast majority of sequences are gibberish/non-compiling code
  • similarly, most random sequences of amino acids are lab-proven (Doug Axe’s work) to be non-functional gibberish
  • the research showing this was conducted at Cambridge University and published in the Journal of Molecular Biology
  • so, random mutation cannot explain the origin of the first living cell
  • however, even natural selection coupled with random mutation cannot explain the first living cell
  • there must already be replication in order for mutation and selection to work, so they can’t explain the first replicator
  • but the origin of life is the origin of the first replicator – there is no replication prior to the first replicator
  • the information in the first replicator cannot be explained by law, such as by chemical bonding affinities
  • the amino acids are attached like magnetic letters on a refrigerator
  • the magnetic force sticks the letters ON the fridge, but they don’t determine the specific sequence of the letters
  • if laws did determine the sequence of letters, then the sequences would be repetitive
  • the three materialist explanations – chance alone, chance and law, law alone – are not adequate to explain the effect
  • the best explanation is that an intelligent cause is responsible for the biological explanation in the first replicator
  • we know that intelligent causes can produce functional sequences of information, e.g. – English, Java code
  • the structure and design of DNA matches up nicely with the design patterns used by software engineers (like WK!)

There are some very good tips in this lecture so that you will be able to explain intelligent design to others in simple ways, using everyday household items and children’s toys to symbolize the amino acids, proteins, sugar phosphate backbones, etc.

Proteins are constructed from a sequence of amino acids:

A sequence of amino acids forming a protein
A sequence of amino acids forming a protein

Proteins sticking onto the double helix structure of DNA:

Some proteins sticking onto the sugar phosphate backbone
Some proteins sticking onto the sugar phosphate backbone

I highly, highly recommend this lecture. You will be delighted and you will learn something.

Here is an article that gives a general overview of how intelligent design challenges. If you want to read something more detailed about the material that he is covering in the lecture above related to the origin of life, there is a pretty good article here.

Related posts

Paul Nelson: the most interesting and significant paper we’ve read in years

Wow, check out this post by Paul Nelson over at Evolution News.

Excerpt:

Now, the paper I retrieved for my co-worker, entitled “The Levinthal paradox of the interactome,” Protein Science 20 (2011):2074-79, explains why the space of “being alive” is so much vastly smaller, and harder to find, than the space of being “not alive.” The paper is short (only six pages) and was written by two structural biologists, Peter Tompa of Vrije Universiteit in Brussels and George Rose of Johns Hopkins University, neither of whom is an intelligent-design advocate. But the paper’s arguments bear so strongly on the design debate, and represent so remarkable a challenge to widely held assumptions about (for instance) the origin of cells, that its effect promises to be far-reaching. As in, revolutionary.

[…]Tompa and Rose draw a number of lessons from their calculations. They argue, first, that any increase in biological realism will only make the Levinthal interactome paradox worse:

Of course, there are additional complicating factors such as alternative splicing, post-translational modifications, non-pairwise macromolecular interactions, incorrect complex formation that is adventitiously stable, and so forth. However, even neglecting such complications, the numbers preclude formation of a functional interactome by trial and error complex formation within any meaningful span of time. This numerical exercise…is tantamount to a proof that the cell does not organize by random collisions of its interacting constituents.But secondly, what they call “the most profound conclusion” from their analysis bears directly on widely held assumptions about the origin of life.

A highly enriched soup of proteins and nucleic acids will never form a functional cell, even if lipid bilayer membranes were provided to help these materials become organized. Indeed, the fully functional contents of a living cell, once the wall or membrane enclosing them has been breached (thus, killing the cell), move irreversibly in the direction of non-living chemistry. Humpty Dumpty, once he cracks, does not reconstitute, but enters what Tompa and Rose call the “zone of chaos,” never to return.

Tompa and Rose have sketched the theoretical basis for why this happens:

[O]ur calculations of combinatorial complexity [show] that the emergent interactome could not have self-organized spontaneously from its isolated protein components. Rather, it attains its functional state by templating the interactome of a mother cell and maintains that state by a continuous expenditure of energy. In the absence of a prior framework of existing interactions, it is far more likely that combined cellular constituents would end up in a non-functional, aggregated state, one incompatible with life…The spontaneous origination of a de novo cell has yet to be observed; all extant cells are generated by the division of pre-existing cells that provide the necessary template for perpetuation of the interactome.

Tompa and Rose spell out other implications of their analysis (e.g., for medicine and synthetic biology), but maybe we’ve piqued your curiosity enough already. This paper deserves your attention. As noted, for a close circle of us at Discovery and Biologic, it’s the most interesting and significant paper we’ve read in years.

Dr. Nelson’s post explains a bit more with pictures.

Doug Axe explains the chances of getting a functional protein by chance

I’ve talked about Doug Axe before when I described how to calculate the odds of getting functional proteins by chance.

Let’s calculate the odds of building a protein composed of a functional chain of 100 amino acids, by chance. (Think of a meaningful English sentence built with 100 scrabble letters, held together with glue)

Sub-problems:

  • BONDING: You need 99 peptide bonds between the 100 amino acids. The odds of getting a peptide bond is 50%. The probability of building a chain of one hundred amino acids in which all linkages involve peptide bonds is roughly (1/2)^99 or 1 chance in 10^30.
  • CHIRALITY: You need 100 left-handed amino acids. The odds of getting a left-handed amino acid is 50%. The probability of attaining at random only L–amino acids in a hypothetical peptide chain one hundred amino acids long is (1/2)^100 or again roughly 1 chance in 10^30.
  • SEQUENCE: You need to choose the correct amino acid for each of the 100 links. The odds of getting the right one are 1 in 20. Even if you allow for some variation, the odds of getting a functional sequence is (1/20)^100 or 1 in 10^65.

The final probability of getting a functional protein composed of 100 amino acids is 1 in 10^125. Even if you fill the universe with pre-biotic soup, and react amino acids at Planck time (very fast!) for 14 billion years, you are probably not going to get even 1 such protein. And you need at least 100 of them for minimal life functions, plus DNA and RNA.

Research performed by Doug Axe at Cambridge University, and published in the peer-reviewed Journal of Molecular Biology, has shown that the number of functional amino acid sequences is tiny:

Doug Axe’s research likewise studies genes that it turns out show great evidence of design. Axe studied the sensitivities of protein function to mutations. In these “mutational sensitivity” tests, Dr. Axe mutated certain amino acids in various proteins, or studied the differences between similar proteins, to see how mutations or changes affected their ability to function properly. He found that protein function was highly sensitive to mutation, and that proteins are not very tolerant to changes in their amino acid sequences. In other words, when you mutate, tweak, or change these proteins slightly, they stopped working. In one of his papers, he thus concludes that “functional folds require highly extraordinary sequences,” and that functional protein folds “may be as low as 1 in 10^77.”

The problem of forming DNA by sequencing nucleotides faces similar difficulties. And remember, mutation and selection cannot explain the origin of the first sequence, because mutation and selection require replication, which does not exist until that first living cell is already in place.

But you can’t show that to your friends, you need to send them a video. And I have a video!

A video of Doug Axe explaining the calculation

Here’s a clip from Illustra Media’s new ID DVD “Darwin’s Dilemma”, which features Doug Axe and Stephen Meyer (both with Ph.Ds from Cambridge University).

I hope you all read Brian Auten’s review of Darwin’s Dilemma! It was awesome.

Related DVDs

Illustra also made two other great DVDs on intelligent design. The first two DVDs “Unlocking the Mystery of Life” and “The Privileged Planet” are must-buys, but you can watch them on youtube if you want, for free.

Here are the 2 playlists:

I also recommend Coldwater Media’s “Icons of Evolution”. All three of these are on sale from Amazon.com.

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