Evidence map›Paper›PMID 17988397›Full record

ArticleBMC evolutionary biology2007

The limits of subfunctionalization.

Thomas MacCarthy, Aviv Bergman

Abstract read
In one paragraph

Article in BMC evolutionary biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

26 citing papers in PubMed.

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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

2 authors.

Thomas MacCarthyDepartment of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, USA. tmaccart@aecom.yu.edu
Aviv Bergman

Funding

A Systems Methodology for the Biology of AgingR01AG028872 · NIA · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI BERGMAN, AVIV · 2007 to 2011
$1.8M
NIA NIH HHS 1-R01-AG028872-01A1NIA NIH HHS R01 AG028872
6 · The paper itself

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.

Indexed as

Evolution, MolecularGene DuplicationGene Expression RegulationGene Regulatory NetworksModels, Genetic

Identifiers

PMID17988397
PMCPMC2213666

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.