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Indel driven rapid evolution of core nuclear pore protein gene promoters
Nuclear pore proteins (Nups) prominently are among the few genes linked to speciation from hybrid incompatibility in Drosophila. These studies have focused on coding sequence evolution of Nup96 and Nup160 and shown evidence of positive selection driving nucleoporin evolution. Intriguingly, channel N...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10192361/ https://www.ncbi.nlm.nih.gov/pubmed/37198214 http://dx.doi.org/10.1038/s41598-023-34985-0 |
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author | McQuarrie, David W. J. Read, Adam M. Stephens, Frannie H. S. Civetta, Alberto Soller, Matthias |
author_facet | McQuarrie, David W. J. Read, Adam M. Stephens, Frannie H. S. Civetta, Alberto Soller, Matthias |
author_sort | McQuarrie, David W. J. |
collection | PubMed |
description | Nuclear pore proteins (Nups) prominently are among the few genes linked to speciation from hybrid incompatibility in Drosophila. These studies have focused on coding sequence evolution of Nup96 and Nup160 and shown evidence of positive selection driving nucleoporin evolution. Intriguingly, channel Nup54 functionality is required for neuronal wiring underlying the female post-mating response induced by male-derived sex-peptide. A region of rapid evolution in the core promoter of Nup54 suggests a critical role for general transcriptional regulatory elements at the onset of speciation, but whether this is a general feature of Nup genes has not been determined. Consistent with findings for Nup54, additional channel Nup58 and Nup62 promoters also rapidly accumulate insertions/deletions (indels). Comprehensive examination of Nup upstream regions reveals that core Nup complex gene promoters accumulate indels rapidly. Since changes in promoters can drive changes in expression, these results indicate an evolutionary mechanism driven by indel accumulation in core Nup promoters. Compensation of such gene expression changes could lead to altered neuronal wiring, rapid fixation of traits caused by promoter changes and subsequently the rise of new species. Hence, the nuclear pore complex may act as a nexus for species-specific changes via nucleo-cytoplasmic transport regulated gene expression. |
format | Online Article Text |
id | pubmed-10192361 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-101923612023-05-19 Indel driven rapid evolution of core nuclear pore protein gene promoters McQuarrie, David W. J. Read, Adam M. Stephens, Frannie H. S. Civetta, Alberto Soller, Matthias Sci Rep Article Nuclear pore proteins (Nups) prominently are among the few genes linked to speciation from hybrid incompatibility in Drosophila. These studies have focused on coding sequence evolution of Nup96 and Nup160 and shown evidence of positive selection driving nucleoporin evolution. Intriguingly, channel Nup54 functionality is required for neuronal wiring underlying the female post-mating response induced by male-derived sex-peptide. A region of rapid evolution in the core promoter of Nup54 suggests a critical role for general transcriptional regulatory elements at the onset of speciation, but whether this is a general feature of Nup genes has not been determined. Consistent with findings for Nup54, additional channel Nup58 and Nup62 promoters also rapidly accumulate insertions/deletions (indels). Comprehensive examination of Nup upstream regions reveals that core Nup complex gene promoters accumulate indels rapidly. Since changes in promoters can drive changes in expression, these results indicate an evolutionary mechanism driven by indel accumulation in core Nup promoters. Compensation of such gene expression changes could lead to altered neuronal wiring, rapid fixation of traits caused by promoter changes and subsequently the rise of new species. Hence, the nuclear pore complex may act as a nexus for species-specific changes via nucleo-cytoplasmic transport regulated gene expression. Nature Publishing Group UK 2023-05-17 /pmc/articles/PMC10192361/ /pubmed/37198214 http://dx.doi.org/10.1038/s41598-023-34985-0 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article McQuarrie, David W. J. Read, Adam M. Stephens, Frannie H. S. Civetta, Alberto Soller, Matthias Indel driven rapid evolution of core nuclear pore protein gene promoters |
title | Indel driven rapid evolution of core nuclear pore protein gene promoters |
title_full | Indel driven rapid evolution of core nuclear pore protein gene promoters |
title_fullStr | Indel driven rapid evolution of core nuclear pore protein gene promoters |
title_full_unstemmed | Indel driven rapid evolution of core nuclear pore protein gene promoters |
title_short | Indel driven rapid evolution of core nuclear pore protein gene promoters |
title_sort | indel driven rapid evolution of core nuclear pore protein gene promoters |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10192361/ https://www.ncbi.nlm.nih.gov/pubmed/37198214 http://dx.doi.org/10.1038/s41598-023-34985-0 |
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