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Analyses of Nuclearly Encoded Mitochondrial Genes Suggest Gene Duplication as a Mechanism for Resolving Intralocus Sexually Antagonistic Conflict in Drosophila
Gene duplication is probably the most important mechanism for generating new gene functions. However, gene duplication has been overlooked as a potentially effective way to resolve genetic conflicts. Here, we analyze the entire set of Drosophila melanogaster nuclearly encoded mitochondrial duplicate...
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Formato: | Texto |
Lenguaje: | English |
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Oxford University Press
2010
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2995371/ https://www.ncbi.nlm.nih.gov/pubmed/21037198 http://dx.doi.org/10.1093/gbe/evq069 |
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author | Gallach, Miguel Chandrasekaran, Chitra Betrán, Esther |
author_facet | Gallach, Miguel Chandrasekaran, Chitra Betrán, Esther |
author_sort | Gallach, Miguel |
collection | PubMed |
description | Gene duplication is probably the most important mechanism for generating new gene functions. However, gene duplication has been overlooked as a potentially effective way to resolve genetic conflicts. Here, we analyze the entire set of Drosophila melanogaster nuclearly encoded mitochondrial duplicate genes and show that both RNA- and DNA-mediated mitochondrial gene duplications exhibit an unexpectedly high rate of relocation (change in location between parental and duplicated gene) as well as an extreme tendency to avoid the X chromosome. These trends are likely related to our observation that relocated genes tend to have testis-specific expression. We also infer that these trends hold across the entire Drosophila genus. Importantly, analyses of gene ontology and functional interaction networks show that there is an overrepresentation of energy production-related functions in these mitochondrial duplicates. We discuss different hypotheses to explain our results and conclude that our findings substantiate the hypothesis that gene duplication for male germline function is likely a mechanism to resolve intralocus sexually antagonistic conflicts that we propose are common in testis. In the case of nuclearly encoded mitochondrial duplicates, our hypothesis is that past sexually antagonistic conflict related to mitochondrial energy function in Drosophila was resolved by gene duplication. |
format | Text |
id | pubmed-2995371 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-29953712010-12-01 Analyses of Nuclearly Encoded Mitochondrial Genes Suggest Gene Duplication as a Mechanism for Resolving Intralocus Sexually Antagonistic Conflict in Drosophila Gallach, Miguel Chandrasekaran, Chitra Betrán, Esther Genome Biol Evol Research Articles Gene duplication is probably the most important mechanism for generating new gene functions. However, gene duplication has been overlooked as a potentially effective way to resolve genetic conflicts. Here, we analyze the entire set of Drosophila melanogaster nuclearly encoded mitochondrial duplicate genes and show that both RNA- and DNA-mediated mitochondrial gene duplications exhibit an unexpectedly high rate of relocation (change in location between parental and duplicated gene) as well as an extreme tendency to avoid the X chromosome. These trends are likely related to our observation that relocated genes tend to have testis-specific expression. We also infer that these trends hold across the entire Drosophila genus. Importantly, analyses of gene ontology and functional interaction networks show that there is an overrepresentation of energy production-related functions in these mitochondrial duplicates. We discuss different hypotheses to explain our results and conclude that our findings substantiate the hypothesis that gene duplication for male germline function is likely a mechanism to resolve intralocus sexually antagonistic conflicts that we propose are common in testis. In the case of nuclearly encoded mitochondrial duplicates, our hypothesis is that past sexually antagonistic conflict related to mitochondrial energy function in Drosophila was resolved by gene duplication. Oxford University Press 2010 2010-10-29 /pmc/articles/PMC2995371/ /pubmed/21037198 http://dx.doi.org/10.1093/gbe/evq069 Text en © The Author(s) 2010. Published by Oxford University Press on behalf of the Society for Molecular Biology and Evolution. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Articles Gallach, Miguel Chandrasekaran, Chitra Betrán, Esther Analyses of Nuclearly Encoded Mitochondrial Genes Suggest Gene Duplication as a Mechanism for Resolving Intralocus Sexually Antagonistic Conflict in Drosophila |
title | Analyses of Nuclearly Encoded Mitochondrial Genes Suggest Gene Duplication as a Mechanism for Resolving Intralocus Sexually Antagonistic Conflict in Drosophila |
title_full | Analyses of Nuclearly Encoded Mitochondrial Genes Suggest Gene Duplication as a Mechanism for Resolving Intralocus Sexually Antagonistic Conflict in Drosophila |
title_fullStr | Analyses of Nuclearly Encoded Mitochondrial Genes Suggest Gene Duplication as a Mechanism for Resolving Intralocus Sexually Antagonistic Conflict in Drosophila |
title_full_unstemmed | Analyses of Nuclearly Encoded Mitochondrial Genes Suggest Gene Duplication as a Mechanism for Resolving Intralocus Sexually Antagonistic Conflict in Drosophila |
title_short | Analyses of Nuclearly Encoded Mitochondrial Genes Suggest Gene Duplication as a Mechanism for Resolving Intralocus Sexually Antagonistic Conflict in Drosophila |
title_sort | analyses of nuclearly encoded mitochondrial genes suggest gene duplication as a mechanism for resolving intralocus sexually antagonistic conflict in drosophila |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2995371/ https://www.ncbi.nlm.nih.gov/pubmed/21037198 http://dx.doi.org/10.1093/gbe/evq069 |
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