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doi:10.1534/genetics.108.090936
A more recent version of this article appeared on August 1, 2008.
NOTE |
Gene dosage and gene duplicability
Wenfeng Qian 1 and Jianzhi Zhang 1*
1 University of Michigan
* To whom correspondence should be addressed. E-mail: jianzhi{at}umich.edu.
Submitted on May 2, 2008
Revised on May 30, 2008
Accepted on 3 June 2008
The evolutionary process leading to the fixation of newly duplicated genes is not well understood. It was recently proposed that the fixation of duplicate genes is frequently driven by positive selection for increased gene dosage (i.e., the gene dosage hypothesis), because haploinsufficient genes were reported to have more paralogs than haplosufficient genes in the human genome. However, the previous analysis incorrectly assumed that the presence of dominant abnormal alleles of a human gene means that the gene is haploinsufficient, ignoring the fact that many dominant abnormal alleles arise from gain-of-function mutations. Here we show in both human and yeast that haploinsufficient genes generally do not duplicate more frequently than haplosufficient genes. Yeast haploinsufficient genes do exhibit enhanced retention after whole genome duplication compared to haplosufficient genes if they encode members of stable protein complexes, but the same phenomenon is absent if the genes do not encode protein complex members, suggesting that the dosage balance effect rather than the dosage effect is the underlying cause of the phenomenon. Based on these and other results, we conclude that selection for higher gene dosage does not play a major role in driving the fixation of duplication genes.
Key Words: dosage balance, duplicability, evolution, gene dosage, gene duplication
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