Godspell Follies

Refuting the illogic of "intelligent design" and creationism. An illustrated guide to fallacies of logic.

Reducible complexity

The contribution of intelligent design advocate, biochemist Michael Behe consists solely of the scientifically refuted notion that a multicomponent functional system cannot have arisen by "Darwinian" evolution. In essence, Behe argues that because removal of any component will render the system non-functional, such a system could not be produced by continuously improving the initial function (which continues to work by the same mechanism) by slight, successive modifications of a precursor system (p.39 of Darwin's Black Box: The Biochemical Challenge to Evolution). Behe targetted several complex systems as purportedly providing support for this flawed proposal: evolution of the eye, clotting cascades and complement system, and the bacterial flagellum.

There are major problems with Michael Behe's contrived challenge of 'irreducible complexity'.
First, the implicit assumption that the components of currently functional system have 'always and only' performed the function that they currently display. The most obvious illustration of this flaw lies in an examination of Behe's for-the-scientifically-ignorant analogy of a spring-based mouse trap. All the components of a spring-based mouse trap can be found, in modified forms, functioning in a variety of settings. It is only the assemblage of these modified forms within a mouse trap that renders each a necessary component of the trap's function. (Intelligent design devotees seem incapable of grasping the point that analogies are useful in explanatory descriptions, but that fallacious arguments from analogy are rapidly invalidated as arguments aimed at attacking scientific facts.) Second, research in medical genetics has uncovered mechanisms that explain 'reducible' complexity. Third, research has demonstrated that assembly of pre-existing modifications operate in subsequently evolved features.

Inherited epigenetic variation--revisiting soft inheritance..
Phenotypic variation is traditionally parsed into components that are directed by genetic and environmental variation. The line between these two components is blurred by inherited epigenetic variation, which is potentially sensitive to environmental inputs. Chromatin and DNA methylation-based mechanisms mediate a semi-independent epigenetic inheritance system at the interface between genetic control and the environment. Should the existence of inherited epigenetic variation alter our thinking about evolutionary change?
Richards EJ. Inherited epigenetic variation--revisiting soft inheritance. Nat Rev Genet. 2006 May;7(5):395-401.

Insights into the spliceosome suggest new explanations for generating biological complexity. modified, hyperlinks inserted:
While politicians debate whether evolution occurs, scientists are busy debating how it occurs. . . .there are more ways than previously thought to achieve the impressive complexity characteristic of humans. Many organisms — including humans — evolve in part by using a complex mechanism by which strands of RNA are spliced together in a two-step process, and delicate balancing of the way this process is executed can generate an enormous number of new gene products, providing a vast reservoir of material for selection during evolution. . . between the “important” coding sections of RNA lie non-coding patches — introns — and as RNA is made it’s the job of a cellular machine called the spliceosome to chop the introns out and splice the rest of the coding sections back together. . . the two steps in this process require the spliceosome to change its shape, flipping back and forth between two distinct conformations. . . Changes in the balance between these two states — referred to as equilibrium — will cause the spliceosome to dwell longer in one conformation at the cost of the other, improving one of the two steps of splicing, to the detriment of the other step. Mutations either in spliceosomal components or in the intron RNA strands can change how the RNA and the spliceosome interact with one another and thus affect the equilibrium. . . there are an abundance of mutated intron splice sites in human DNA, also called alternative splice sites. . . when the equilibrium of the spliceosome is changed — either because the mutated splice sites interact with it differently or because other accessory molecules bind to the spliceosome — they can be recognized and spliced. The utilization of alternative splice sites allows for different combinations of coding RNA sequences to be put together, so that one RNA transcript can make a variety of different products, each with a potentially different function. This explains why, when the human genome was first sequenced, relatively few genes were found. . . This has allowed our genome to develop in complexity.”
Molecular Cell 21(4): 543-553 (February 17, 2006)

Lenski et al have demonstrated that complex features can evolve by expanding earlier, simpler functions, and that an intermediate stage is not necessary for this evolution. Thus, they have demonstrated how to reconstruct a complete evolutionary history of a complex genetically encoded function. Their computations vindicate Darwin's idea that the target of natural selection constantly changes, and that the complex feature of today may share very little with the original function. Darwin wrote, "if we look to an organ common to all the members of a large class in order to discover the early transitional grades through which the organ has passed, we should have to look to very ancient ancestral forms, long since become extinct."

The work of Lenski et al and the experiments of Bridgham et al (below) demonstrate that Behe's contrived challenge to Darwinian evolution, namely "irreducible complexity", is not a valid criticism of the mechanisms of evolution. The two groups have demonstrated that complex systems can evolve and lend disproof to the claim that complex systems must have been designed.

The evolutionary origin of complex features.
A long-standing challenge to evolutionary theory has been whether it can explain the origin of complex organismal features. We examined this issue using digital organisms--computer programs that self-replicate, mutate, compete and evolve. Populations of digital organisms often evolved the ability to perform complex logic functions requiring the coordinated execution of many genomic instructions. Complex functions evolved by building on simpler functions that had evolved earlier, provided that these were also selectively favoured. However, no particular intermediate stage was essential for evolving complex functions. The first genotypes able to perform complex functions differed from their non-performing parents by only one or two mutations, but differed from the ancestor by many mutations that were also crucial to the new functions. In some cases, mutations that were deleterious when they appeared served as stepping-stones in the evolution of complex features. These findings show how complex functions can originate by random mutation and natural selection.
Lenski RE, Ofria C, Pennock RT, Adami C. The evolutionary origin of complex features. Nature. 2003 May 8;423(6936):139-44.

Lock before Key: Entrez PubMed: "According to Darwinian theory, complexity evolves by a stepwise process of elaboration and optimization under natural selection. Biological systems composed of tightly integrated parts seem to challenge this view, because it is not obvious how any element's function can be selected for unless the partners with which it interacts are already present. Here we demonstrate how an integrated molecular system-the specific functional interaction between the steroid hormone aldosterone and its partner the mineralocorticoid receptor-evolved by a stepwise Darwinian process. Using ancestral gene resurrection, we show that, long before the hormone evolved, the receptor's affinity for aldosterone was present as a structural by-product of its partnership with chemically similar, more ancient ligands. Introducing two amino acid changes into the ancestral sequence recapitulates the evolution of present-day receptor specificity. Our results indicate that tight interactions can evolve by molecular exploitation-recruitment of an older molecule, previously constrained for a different role, into a new functional complex."

Bridgham JT, Carroll SM, Thornton JW. Evolution of hormone-receptor complexity by molecular exploitation. Science. 2006 Apr 7;312(5770):97-101.
Comment in: Science. 2006 Apr 7;312(5770):61-3.

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