. . . Force, A., M. Lynch, F.B. Pickett, A. Amores, Y.-L. Yan, and J. Postlethwait.
The preservation of duplicate genes by complementary degenerative mutations. Genetics 151:1531-1545. 1999.
Gene duplication is commonly given as the explanation for the increase in complexity via the acquisition of new functions. This paper addresses the standard scenario of duplication followed by either an adaptive mutation leading to the preservation of both genes or followed by degeneration of one of the copies. Since detrimental mutations are more likely than benificial mutations, the classical model predict that one of the duplicated genes will become a psuedogene. Actual data seems to indicate that the number of functional copies is larger than expected from the classical model and the authors present an interesting alternative. The alternative explains duplicate gene preservation by the fixation of a degenerative mutation rather than a more rare benificial mutations. The authors also present data from the Zebrafish consistent with this new model.
ABSTRACT The origin of organismal complexity is generally thought to be tightly coupled to the evolution of new gene functions arising subsequent to gene duplication. Under the classical model for the evolution of duplicate genes, one member of the duplicated pair usually degenerates within a few million years by accumulating deleterious mutations, while the other duplicate retains the original function. This model further predicts that on rare occasions, one duplicate may acquire a new adaptive function, resulting in the preservation of both members of the pair, one with the new function and the other retaining the old. However, empirical data suggest that a much greater proportion of gene duplicates is preserved than predicted by the classical model. Here we present a new conceptual framework for understanding the evolution of duplicate genes that may help explain this conundrum. Focusing on the regulatory complexity of eukaryotic genes, we show how complementary degenerative mutations in different regulatory elements of duplicated genes can facilitate the preservation of both duplicates, thereby increasing long-term opportunities for the evolution of new gene functions. The duplication-degeneration-complementation (DDC) model predicts that (1) degenerative mutations in regulatory elements can increase rather than reduce the probability of duplicate gene preservtion and (2) the usual mechanism of duplicate gene preservation is the partitioning of ancestral functions rather than the evolution of new functions. We present several examples (including analysis of a new engrailed gene in zebrafish) that appear to be consistent with the DDC model, and we suggest several analytical and experimental approaches for determining whether the complementary loss of gene subfunctions or the acquisition of novel functions are likely to be the primary mechanisms for the preservation of gene duplicates.