Other improvements of the basic model for duplicated gene retention, involving buffering of crucial functions via conversion and crossing-over, were recently proposed [ 8, 9].
To date, mechanistic models for duplicate gene retention only account for the mutation-driven nonfunctionalization process.
Several models for duplicate gene retention and subsequent fates have been proposed, including genetic redundancy, gene dosage balance, genetic robustness, and divergence of protein sequence and expression patterns that can lead to neofunctionalization, subfunctionalization, or subcellular relocalization (reviewed in Sémon and Wolfe 2007; Hahn 2009; Innan and Kondrashov 2010).
(with Timothy P. Walter) "A simulation model for purchasing duplicate copies in a library". Journal of Library Automation 7 73-82.
This implies that a substantial fraction of gene duplicates may not meet the standard of functional equivalency at birth, an integral component of Ohno's model for gene duplicate evolution and diversification [ 14].
In the gene conservation model for gene duplicate retention the paralogues retain the original function of the ancestral gene and the evolutionary advantage is to increase gene copy number [ 22].
In dosage-compensated duplicates, network interactions can be lost through nonfunctionalization of entire genes or through loss of individual interactions, which when lost complementarily will result in subfunctionalization. Models for gene duplicate retention enable insight into the evolution of protein function following speciation and lineage-specific evolution.
These were obtained either from the Zebra finch Ensembl model, or by mapping the Zebra finch parent gene and its chicken ortholog onto the novel gene locus, in cases where an Ensembl model for the novel duplicate was absent or incomplete (in the latter case noting the possible occurrence of additional unmapped exons/domains in nearby regions).
Differential induction of only one of the sister pair of duplicated fabp genes by FAs provides evidence to support the DDC model for retention of duplicated genes in the zebrafish genome by either subfunctionalization or neofunctionalization.
The most well known model of this type is the neutral sub-functionalization model for the promulgation of duplicate genes proposed independently by Stoltzfus [ 7] and by Force, Lynch, et al. [ 12, 13], who refer to it as the duplication-degeneration-complementation (DDC) model.
