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A New Gene Fits in Without a Ripple

A recent paper in Science, “Stepwise Evolution of Essential Centromere Function in a Drosophila Neogene,” examined a modified-duplicate gene in a species of fruit fly and concluded that it developed a vital role in the organism within the past 15 million years. The authors think that their work may contribute to our understanding of how some relatively new genes are folded into the cell’s machinery and become essential over time. I think they’re right, as far as that goes. What the work doesn’t show, however, is how Darwinian processes might lead to a new, functionally complex (let alone irreducibly complex) system.

Ross et al (2013) investigated the gene dubbed Umbrea, which is a modified duplicate of a gene called HP1B. They showed that, whereas HP1B codes for a protein that associates with chromatin, Umbrea localizes to interphase centromeres. What’s more, although the parent gene is dispensable, the modified duplicate gene is vital in one species (D. melanogaster) — fruit flies missing the new gene die before fully developing.

The authors looked at gene regions of 32 species of the genus Drosophila. One grouping of species does not have the duplicate gene while another one does, indicating that the gene duplicated after the two groupings split in the past. Within the grouping that has the duplicate about a fifth of species have a full copy of the old gene, about three-fifths have lost a chunk of the gene called the CSD-coding region, and another fifth have lost the duplicate gene entirely. The authors think this checkered history points to a single gene duplication plus multiple episodes of loss, until Umbrea acquired several mutations leading to amino acid changes, which conferred on the truncated protein the ability to bind near centromeres. Apparently other changes then made the developmental apparatus of the fruit fly dependent on the new protein such that removing it is now lethal.

I have no reason to doubt this scenario. However, it may be useful to point out what the results do not indicate. First, as the authors acknowledge, the “new” gene isn’t a brand-new gene — it’s a modified duplicate of an old one, which itself coded for a fully functioning protein. Second, the current function of the Umbrea protein is not known (nor is the function of the original protein). Thus any conclusions about how easy or difficult the pathway from the original to the derivative protein are speculative. Third, the changes needed to make the descendant protein bind to a new partner apparently are modifications of the protein-binding site of the original. Thus, while this makes it a gain-of-function mutation in my view, such gains of function do happen sporadically by Darwinian means, as I have reviewed, and the current one appears to be rather modest. Fourth, the changes occurred in the genus Drosophila, which has a huge population size and a rapid generation time. Thus it has the population resources that allow for the occasional very rare mutation.

Last, the essentiality or non-essentiality of a gene has nothing to do with the complexity of a system. A gene can be essential for life and yet not part of a complex protein system (such as hemoglobin). And a gene can be non-essential and part of a functioning complex system (such as the genes coding for parts of the bacterial flagellum, which is dispensable for cell viability). The major task for a theory of life is to explain the origin of complex functional systems, which intelligent design alone does easily.

Although there is not yet enough information for a definitive conclusion, the system investigated by Ross et al (2013) appears to be a simple case of “genomic drift,” where modest changes meander through the genomes of large populations over time, altering the organism very little.

References:

Ross, B.D., Rosin, L., Thomae, A.W., Hiatt, M.A., Vermaak, D., de la Cruz, A.F., Imhof, A., Mellone, B.G., and Malik, H.S. 2013. Stepwise evolution of essential centromere function in a Drosophila neogene. Science 340:1211-1214.

Behe, M.J. 2010. Experimental Evolution, Loss-of-function Mutations, and “The First Rule of Adaptive Evolution.” Q. Rev. Biol. 85:1-27.

Image credit: Not So Much/Flickr.

Michael J. Behe

Senior Fellow, Center for Science and Culture
Michael J. Behe is Professor of Biological Sciences at Lehigh University in Pennsylvania and a Senior Fellow at Discovery Institute’s Center for Science and Culture. He received his Ph.D. in Biochemistry from the University of Pennsylvania in 1978. Behe's current research involves delineation of design and natural selection in protein structures. In his career he has authored over 40 technical papers and three books, Darwin Devolves: The New Science About DNA that Challenges Evolution, Darwin’s Black Box: The Biochemical Challenge to Evolution, and The Edge of Evolution: The Search for the Limits of Darwinism, which argue that living system at the molecular level are best explained as being the result of deliberate intelligent design.

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