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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).
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A general model for duplicate gene loss/retention is then presented that is capable of fitting expectations under the different models, is defined at t = 0, and decays to an orthologous asymptotic rate rather than zero, based upon a modified Weibull hazard function.
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].
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.
(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].
There are a number of models for the fate of duplicate gene that predict functional differentiation of paralogs based on protein sequence or regulatory divergence [ 24, 25].
The reconstructed metabolic models contain duplicate genes for the same reaction, or alternative reactions between two metabolites, or alternative pathways among metabolites.
The fate of duplicated gene copies has been amply discussed and several models have been put forward to account for duplicate conservation.
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