May 15, 2005 | David F. Coppedge

Can Gene Duplication Promote Evolution?

Imagine you had no mouth but needed to eat.  A hamburger comes flying at you.  When it hits your body, your skin folds around it and pinches off, sealing it inside.  Dozens of 3-armed parts form a geodesic dome around it and carry it to the stomach.  Once delivered, all the parts are recycled for the incoming freedom fries.
    If this sounds bizarre, it’s kind of what really happens in your cells.  Except for specialized channels that accept particular molecules, like water (12/20/2001 and salt (01/17/2002), a cell has no mouth; it is surrounded by a continuous membrane.  When large nutrients need to get in, the membrane has acceptors on the outside that signal a cascade of events.  The membrane dents inward and envelops the particle.  On the inside, proteins called clathrins form a geodesic structure around the incoming vesicle as the membrane pinches off and seals the contents inside.  Other proteins and enzymes stand at the ready to deliver the nutrient where needed.  This process goes on continually and is called endocytosis.  A press release from the University of Queensland says the cell eats its entire skin every 30 minutes.
    Progress continues to be made understanding clathrin-mediated endocytosis since our 10/07/2003 entry, but the evolutionary origin of this elegant system seems illusory.  UC and Stanford biochemists writing in PNAS1 noted that two forms of clathrin are so different, being coded by different genes, they must have had separate evolutionary histories.  They propose this happened during gene duplication events up to 600 million years ago.
    Andreas Wagner, however, publishing in Molecular Biology and Evolution,2 casts doubt on that method of evolutionary change:

I here estimate the energy cost of changes in gene expression for several thousand genes in the yeast Saccharomyces cerevisiaeA doubling of gene expression, as it occurs in a gene duplication event, is significantly selected against for all genes for which expression data is available.  It carries a median selective disadvantage of s > 10�5, several times greater than the selection coefficient s = 1.47 x 10�7 below which genetic drift dominates a mutant’s fate.  When considered separately, increases in messenger RNA expression or protein expression by more than a factor 2 also have significant energy costs for most genes.  This means that the evolution of transcription and translation rates is not an evolutionarily neutral process.  They are under active selection opposing them.  My estimates are based on genome-scale information of gene expression in the yeast S. cerevisiae as well as information on the energy cost of biosynthesizing amino acids and nucleotides.   (Emphasis added in all quotes.)

Whatever the origin of clathrin, its reputation as a versatile molecule is growing.  In the April 28 issue of Nature,3 three Cambridge biologists wondered what it does when endocytosis is halted during cell division.  They discovered that clathrin has another essential job:

Clathrin has an established function in the generation of vesicles that transfer membrane and proteins around the cell.  The formation of clathrin-coated vesicles occurs continuously in non-dividing cells, but is shut down during mitosis, when clathrin concentrates at the spindle apparatus.  Here, we show that clathrin stabilizes fibres of the mitotic spindle to aid congression of chromosomes.  Clathrin bound to the spindle directly by the amino-terminal domain of clathrin heavy chain.  Depletion of clathrin heavy chain using RNA interference prolonged mitosis; kinetochore fibres were destabilized, leading to defective congression of chromosomes to the metaphase plate and persistent activation of the spindle checkpoint.  Normal mitosis was rescued by clathrin triskelia [complete 3-part clathrin proteins] but not the N-terminal domain of clathrin heavy chain, indicating that stabilization of kinetochore fibres was dependent on the unique structure of clathrin.

This is not just an incidental task for clathrin to do till cell division is over.  “The importance of clathrin for normal mitosis,” they say, “may be relevant to understanding human cancers that involve gene fusions of clathrin heavy chain.”

1Wakeham et al., “Clathrin heavy and light chain isoforms originated by independent mechanisms of gene duplication during chordate evolution,” Proceedings of the National Academy of Sciences USA, 10.1073/pnas.0502058102, published online before print May 9, 2005.
2Andreas Wagner, “Energy Constraints on the Evolution of Gene Expression,” Molecular Biology and Evolution, 2005 22(6):1365-1374; doi:10.1093/molbev/msi126.
3Royle et al., “Clathrin is required for the function of the mitotic spindle,” Nature 434, 1152-1157 (28 April 2005) | doi: 10.1038/nature03502.

Gene duplication is one of the mechanisms Darwinists invoke when Natural Selection seems inadequate for a job, and they want to make it seem like there are other tricks in the toolkit of Charlie the Magician.  The abstract of Wagner’s paper seems to make it clear that duplication is not going to help.  If two tools are fighting each other, like front and rear tires spinning in opposite directions, the vehicle is not going anywhere.  Now go back and reread the 10/07/2003 entry about endocytosis and see if you think the Darwin Party has a prayer for explaining it.  Be sure to watch Allison Bruce’s cool video of clathrin making geodesic domes.  How many of you would vote for chance and natural selection producing this geometrical marvel?  Someone other than a Darwinist, who not only has a prayer but a Recipient, should get a hearing.

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Categories: Cell Biology

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