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Science Friction_ Where the Known Meets the Unknown - Michael Shermer [111]

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more complex units called eukaryote cells (those little organelles inside cells you had to memorize in beginning biology were once self-contained independent cells); some of these eukaryote cells self-organized into multicellular organisms; some of these multicellular organisms self-organized into such cooperative ventures as colonies and social units. And so forth. We can even think of self-organization as an emergent property, and emergence as a form of self-organization. How recursive. No Intelligent Designer made these things happen. They happened on their own.

As a complex adaptive system the cosmos intelligently designs itself. It is one giant autocatalytic (self-driving) feedback loop that generates emergent properties, one of which is life. There may even be a type of natural selection at work among the many bubble universes, with those whose parameters are like ours most likely to survive. Those bubble universes whose parameters are most likely to give rise to life occasionally generate complex life with brains big enough to achieve consciousness and to conceive of such concepts as God and cosmology and to ask such questions as Why?

7. Explanatory Gaps. ID theory fills in an explanatory gap that science cannot or has not filled. It is legitimate to identify the shortcomings of evolutionary theory, and show how scientists have not, and perhaps cannot, provide examples of evolution at work. It is one thing to infer in the fossil record a speciation event or the creation of a new structure; it is quite another to witness it in the laboratory. It is fair and reasonable to argue that students should be made aware of these explanatory shortcomings on the part of science.

Not only does science have the incredibly rich fossil record, the process of evolution can be seen at work at a number of different levels. We know from genetics that every dog on the planet descended from a single population of wolves in China about 15,000 years ago. Granted, this was a combination of natural selection and artificial selection (breeding), but it also now appears from both genetics and paleontology that every human on the planet descended from a single population of Homo sapiens in Africa about 150,000 years ago. That’s a lot of evolution in a relatively short period of time. And, of course, diseases are prime examples of natural selection and evolution at work, and on timescales we can witness, all too painfully. The AIDS virus, for example, continues to evolve in response to the drugs used to combat it—the few surviving strains of the virus continue to multiply, passing on their drug-resistant genes. This is evolution in action, which was even caught in a laboratory experiment published in the February 20, 2004, edition of Science, in which E. coil bacteria that were forced to adapt or perish improvised a novel molecular tool. According to the experimenter, University of Michigan biologist James Bardwell, “The bacteria reached for a tool that they had, and made it do something it doesn’t normally do. We caught evolution in the act of making a big step.” The big step was a new way of making molecular bolts called disulfide bonds, which are stiffening struts in proteins that also help the proteins fold into their proper, functional, three-dimensional shapes. This new method restarted the bacteria’s motor and enabled it to move toward food before it starved to death.

This is an important experiment because Bardwell had developed a strain of mutant bacteria unable to make disulfide bonds, which are critical for the ability of the bacteria’s propeller-like swimming motor, the flagella, to work. This is the same flagella that creationists are so fond of displaying as examples of irreducible complexity. The researchers put these nonswimming bacteria to the test by placing them on a dish of food where, once they had exhausted the food they could reach, they had to either repair the broken motor or starve to death. The bacteria used in the experiment were forced to use a protein called thioredoxin, which normally destroys disulfide bonds,

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