Journal
GENOME BIOLOGY AND EVOLUTION
Volume 7, Issue 8, Pages 2258-2264Publisher
OXFORD UNIV PRESS
DOI: 10.1093/gbe/evv139
Keywords
gene duplication; fixation; copy number variation; nonfunctionalization
Categories
Funding
- National Science Foundation [NSF DMS-1222940]
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM104040] Funding Source: NIH RePORTER
- Div Of Biological Infrastructure [1300426] Funding Source: National Science Foundation
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Most sequenced eukaryotic genomes show a large excess of recent duplicates. As duplicates age, both the population genetic process of failed fixation and the mutation-driven process of nonfunctionalization act to reduce the observed number of duplicates. Understanding the processes generating the age distributions of recent duplicates is important to also understand the role of duplicate genes in the functional divergence of genomes. To date, mechanistic models for duplicate gene retention only account for the mutation-driven nonfunctionalization process. Here, a neutral model for the distribution of synonymous substitutions in duplicated genes which are segregating and expected to never fix in a population is introduced. This model enables differentiation of neutral loss due to failed fixation from loss due to mutation-driven nonfunctionalization. The model has been validated on simulated data and subsequent analysis with the model on genomic data from human and mouse shows that conclusions about the underlying mechanisms for duplicate gene retention can be sensitive to consideration of population genetic processes.
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