Agents of Biological Design

Scott Turner gave a presentation at Binghamton University’s EvoS speaker’s series in December 2007.  He outlined the argument for biological design that is developed more fully in his book.  You can watch the narrated Power Point version of this talk here: Agents of Biological Design.

The presentation is 42 minutes long and well worth watching.  I especially enjoyed the section starting with slide 16.  If you watch it, it might help you better visualize what I was saying in this blog entry:

This study does not in any way indicate a fundamental flaw in Darwin’s Theory. Nor does it demonstrate that bacteria can target the specific genes needed to survive the environmental insult. What it does do is help us understand that life takes control of its fate. Living things are not passive participants of the interplay between stochastic events and environmental pressures, where mutations that just happened to exist are favored in an environment that just happened to exist. Instead, environmental challenges are met with a truly biotic response. First, the cells try to repair themselves. But if this fails, then they seek out an adaptation by maximizing their chances of finding an adaptation. Evolution is, at least, partially controlled by properties intrinsic to life.

While the teleological echo is faint, it is nevertheless there. We can begin to catch a glimpse of evolution as homeostasis. The integrity of the genome is threatened. Standard small scale feedback responses ensue as the cell attempts to reverse the change through repair and recombination mechanisms. But if the insult is too severe or too common, the next level of feedback response is…..evolution itself. The antibiotic is the stress that perturbs the homeostasis of the cells and evolution is the effector that reverses the effects of the change. Life fights back.

I also enjoyed his physiological perspective on cognition toward the end of the presentation.

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5 responses to “Agents of Biological Design

  1. So lets see the flow of logic here. Life repairs itself, if it can’t “evolution” occurs. Is “evolution” therefore dependent on the first phase of repair? If yes, whats responsible for the initial dependency (signals and feedbacks that trigger “evolution”). Do repair mechanisms evolve to slow down the subsequent “evolution” process, oh is that what “evolution” had in mind? What are the probabilities of evolution occuring given that repair mechanisms steal a chunk of its time to select further?

  2. So lets see the flow of logic here. Life repairs itself, if it can’t “evolution” occurs. Is “evolution” therefore dependent on the first phase of repair?

    It probably depends on the context and what is evolving. In this particular study, the ability to evolve resistance to two antibiotics was dependent on the SOS system. As I wrote at the time:

    The researchers tested two antibiotics: ciprofloxacin, which targets the gyrase and topoisomerase (proteins involved in untangling DNA) and rifampicin, which targets the bacterial RNA polymerase. They found that after 72 hours of continual exposure to ciproflaxin, 3% of the recovered bacteria had acquired resistance to the antibiotic. With 72 hours of exposure to rifampicin, 100% of the bacteria were resistant. However, when they similarly tested a strain that lacked LexA, no antibiotic resistance has found. This led them to conclude “that LexA cleavage is absolutely required for the evolution of resistance to both ciprofloxacin and rifampicin during therapy in vivo.”

    If yes, whats responsible for the initial dependency (signals and feedbacks that trigger “evolution”).

    I think that in many cases, we can view major evolutionary transitions as the ultimate biotic response to stress. Homeostasis is the core principle behind life, so it doesn’t make sense for me to think the influence of homeostasis suddenly stops when it comes to life adapting to the environment and adapting the environment to itself.

    Do repair mechanisms evolve to slow down the subsequent “evolution” process, oh is that what “evolution” had in mind?

    Haven’t really given that one much thought.

    What are the probabilities of evolution occuring given that repair mechanisms steal a chunk of its time to select further?

    Don’t know.

    Anyway, first things first.

    1. The primary focus of this blog entry was to get people to watch Turner’s presentation. Turner also thinks that homeostasis is a player in evolution – he call’s it the Tinkerer’s Accomplice.

    2. As for the LexA study, it is a nice study that shows us evolution is not always a passive process of selection screening through the available variability. And this highlights another serious flaw in the Modern Synthesis.

  3. I think Turner’s criticism of ID was critically flawed. And you know how it is – people love to criticize more than praise, so here I go.

    * He says “Darwin dealt a deathblow to the idea” of a demiurge, but he then turns around and says that consciousness is idiosyncratic, platform-specific, and inscrutable. That’s like saying that idea X has been disproved, and also idea X is impossible to disprove. It can’t be had both ways.

    * That also conflicts with Dembski’s recent claim that ID’s ‘designer’ could be “an intelligent alien, a computional simulator (a la THE MATRIX), a Platonic demiurge, a Stoic seminal reason, an impersonal telic process, …, or the infinite personal transcendent creator God of Christianity?” If he’s using Dembski to decide what ID must be, Turner’s ideas may well fall under that “big tent”.

    That said, I find Turner’s ideas fascinating, and his willingness to discard atomism and take on ‘intentionality’ as apparently fundamental to nature is intriguing. Then again, I’m sympathetic to Aristotilean ideas, and Turner’s seem to fit in well there.

  4. He says “Darwin dealt a deathblow to the idea” of a demiurge, but he then turns around and says that consciousness is idiosyncratic, platform-specific, and inscrutable. That’s like saying that idea X has been disproved, and also idea X is impossible to disprove. It can’t be had both ways.

    Good catch. I’m so used to seeing people do that type of double-dipping that I missed that.

  5. Homeostasis? Rheostasis? Allostasis?

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