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BMC Evolutionary Biology

, 7:213

First Online: 07 November 2007Received: 16 May 2007Accepted: 07 November 2007

Abstract

BackgroundThe duplication-degeneration-complementation DDC model has been proposed as an explanation for the unexpectedly high retention of duplicate genes. The hypothesis proposes that, following gene duplication, the two gene copies degenerate to perform complementary functions that jointly match that of the single ancestral gene, a process also known as subfunctionalization. We distinguish between subfunctionalization at the regulatory level and at the product level e.g within temporal or spatial expression domains.

ResultsIn contrast to what is expected under the DDC model, we use in silico modeling to show that regulatory subfunctionalization is expected to peak and then decrease significantly. At the same time, neofunctionalization recruitment of novel interactions increases monotonically, eventually affecting the regulatory elements of the majority of genes. Furthermore, since this process occurs under conditions of stabilizing selection, there is no need to invoke positive selection. At the product level, the frequency of subfunctionalization is no higher than would be expected by chance, a finding that was corroborated using yeast microarray time-course data. We also find that product subfunctionalization is not necessarily caused by regulatory subfunctionalization.

ConclusionOur results suggest a more complex picture of post-duplication evolution in which subfunctionalization plays only a partial role in conjunction with redundancy and neofunctionalization. We argue that this behavior is a consequence of the high evolutionary plasticity in gene networks.

Electronic supplementary materialThe online version of this article doi:10.1186-1471-2148-7-213 contains supplementary material, which is available to authorized users.

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Author: Thomas MacCarthy - Aviv Bergman

Source: https://link.springer.com/article/10.1186/1471-2148-7-213



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