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Michael Behe Responds To Näsvall et al. (2012)

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Michael Behe has a new blog post at Evolution News & Views responding to this paper that recently appeared in Science:

A paper appeared recently in Science that reminded me of one of my favorite toys when I was a kid — a rolling-ball maze. Over the years I had a few different varieties, including two- and three-dimensional ones. The basic gist is that a person has to twist and turn the toy to roll a ball through a plastic, transparent maze from the entrance to the exit. Of course there are a lot of dead ends and blind alleys, so it’s pretty tricky, at least at first. Once you learn the path, it becomes trivial.

Näsvall et al. (2012) do the same with a protein, manipulating experimental conditions to roll it through dead ends and have it come out in the place they want. Although the printed paper itself and an accompanying commentary by Elizabeth Pennisi paint the results as an advance in understanding evolution, that’s so only if evolution has eyes and a mind like a kid solving a maze. The investigators’ exceptionally intelligent manipulations are relegated to the online supplemental materials.

Read the rest here.

4 Replies to “Michael Behe Responds To Näsvall et al. (2012)

  1. 1
    Axel says:

    Animists are Maccabean in their ferocious loyalty to their gods, Michael.

  2. 2
    Box says:

    Isn’t the production of the ‘protein needed to make the essential amino acid tryptophan’ utterly useless for the bacteria if a regulationary system is lacking? Too much or too little tryptophan is unhealthy, I suppose.
    ‘The essence of cellular life is regulation: The cell controls how much and what kinds of chemicals it makes; when it loses control, it dies’, Michael Behe, Darwin’s black box, p.191.
    If so, did Näsvall et al remove the regulationary system as well?

  3. 3
    Mung says:

    Is there some reason to think that evolution isn’t guided?

  4. 4
    Box says:

    // Backing up Behe’s statements:

    Behe: They deleted an enzyme that previous work showed could likely be replaced.

    Näsvall: Deletion of the trpF and hisA genes.
    The his A and trpF genes were replaced with FLP-recombinase target (FRT) site flanked kanamycin resistance (KanR) cassettes derived from plasmid pKD4, using the lambda-red recombineering functions from plasmid pKD46 (24).

    ***

    Behe: They added the necessary nutrient histidine because previous work showed that mutations conferring an ability to make tryptophan destroyed the ability to make histidine.

    Näsvall: We included histidine in the medium because previous studies have demonstrated that mutations that confer TrpF activity to Thermotoga maritima HisA results in loss of HisA activity (27).

    ***

    Behe: The added histidine would have shut off production of the protein, so they removed the genetic control element to keep it in production.

    Näsvall: The expression of the his operon (including hisA) is regulated by an attenuation mechanism that regulates the amount of read-through of a transcriptional terminator before the first structural gene of the operon according to the availability of charged histidinyl-tRNA (2V). As this results in very low expression of hisA in medium containing histidine, we included a mutation (hisO/242) (29) which removes the transcriptional terminator thereby leading to de-repressed transcription of the his operon even in the presence of histidine.

    [source: supplement]

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