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dc.creatorKonradf, A
dc.creatorTeufelf, AI
dc.creatorGrahnen, JA
dc.creatorLiberles, DA
dc.date.accessioned2021-01-31T23:27:22Z
dc.date.available2021-01-31T23:27:22Z
dc.date.issued2011-12-01
dc.identifier.issn1759-6653
dc.identifier.issn1759-6653
dc.identifier.doihttp://dx.doi.org/10.34944/dspace/5485
dc.identifier.other21920903 (pubmed)
dc.identifier.urihttp://hdl.handle.net/20.500.12613/5503
dc.description.abstractGene duplication is an important process in the functional divergence of genes and genomes. Several processes have been described that lead to duplicate gene retention over different timescales after both smaller-scale events and whole-genome duplication, including neofunctionalization, subfunctionalization, and dosage balance. Two common modes of duplicate gene loss include nonfunctionalization and loss due to population dynamics (failed fixation). Previous work has characterized expectations of duplicate gene retention under the neofunctionalization and subfunctionalization models. Here, that work is extended to dosage balance using simulations. 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. The model in a maximum likelihood framework shows the property of identifiability, recovering the evolutionary mechanism and parameters of simulation. This model is also capable of recovering the evolutionary mechanism of simulation from data generated using an unrelated network population genetic model. Lastly, the general model is applied as part of a mixture model to recent gene duplicates from the Oikopleura dioica genome, suggesting that neofunctionalization may be an important process leading to duplicate gene retention in that organism. © The Author(s) 2010.
dc.format.extent1197-1209
dc.language.isoen
dc.relation.haspartGenome Biology and Evolution
dc.relation.isreferencedbyOxford University Press (OUP)
dc.rightsCC BY-NC
dc.rights.urihttp://creativecommons.org/licenses/by-nc/3.0
dc.subjectdosage balance
dc.subjectgene duplication
dc.subjectneofunctionalization
dc.subjectsubfunctionalization
dc.subjectprotein-protein interaction network
dc.subjectstochastic model
dc.titleToward a general model for the evolutionary dynamics of gene duplicates
dc.typeArticle
dc.type.genreJournal Article
dc.relation.doi10.1093/gbe/evr093
dc.ada.noteFor Americans with Disabilities Act (ADA) accommodation, including help with reading this content, please contact scholarshare@temple.edu
dc.creator.orcidLiberles, David A|0000-0003-3487-8826
dc.date.updated2021-01-31T23:27:18Z
refterms.dateFOA2021-01-31T23:27:23Z


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