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A gene duplication of a septin reveals a developmentally regulated filament length control mechanism
Septins are a family of conserved filament-forming proteins that function in multiple cellular processes. The number of septin genes within an organism varies, and higher eukaryotes express many septin isoforms due to alternative splicing. It is unclear if different combinations of septin proteins i...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Rockefeller University Press
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9960279/ https://www.ncbi.nlm.nih.gov/pubmed/36786832 http://dx.doi.org/10.1083/jcb.202204063 |
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author | Cannon, Kevin S. Vargas-Muniz, Jose M. Billington, Neil Seim, Ian Ekena, Joanne Sellers, James R. Gladfelter, Amy. S. |
author_facet | Cannon, Kevin S. Vargas-Muniz, Jose M. Billington, Neil Seim, Ian Ekena, Joanne Sellers, James R. Gladfelter, Amy. S. |
author_sort | Cannon, Kevin S. |
collection | PubMed |
description | Septins are a family of conserved filament-forming proteins that function in multiple cellular processes. The number of septin genes within an organism varies, and higher eukaryotes express many septin isoforms due to alternative splicing. It is unclear if different combinations of septin proteins in complex alter the polymers’ biophysical properties. We report that a duplication event within the CDC11 locus in Ashbya gossypii gave rise to two similar but distinct Cdc11 proteins: Cdc11a and Cdc1b. CDC11b transcription is developmentally regulated, producing different amounts of Cdc11a- and Cdc11b-complexes in the lifecycle of Ashbya gossypii. Deletion of either gene results in distinct cell polarity defects, suggesting non-overlapping functions. Cdc11a and Cdc11b complexes have differences in filament length and membrane-binding ability. Thus, septin subunit composition has functional consequences on filament properties and cell morphogenesis. Small sequence differences elicit distinct biophysical properties and cell functions of septins, illuminating how gene duplication could be a driving force for septin gene expansions seen throughout the tree of life. |
format | Online Article Text |
id | pubmed-9960279 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-99602792023-08-14 A gene duplication of a septin reveals a developmentally regulated filament length control mechanism Cannon, Kevin S. Vargas-Muniz, Jose M. Billington, Neil Seim, Ian Ekena, Joanne Sellers, James R. Gladfelter, Amy. S. J Cell Biol Article Septins are a family of conserved filament-forming proteins that function in multiple cellular processes. The number of septin genes within an organism varies, and higher eukaryotes express many septin isoforms due to alternative splicing. It is unclear if different combinations of septin proteins in complex alter the polymers’ biophysical properties. We report that a duplication event within the CDC11 locus in Ashbya gossypii gave rise to two similar but distinct Cdc11 proteins: Cdc11a and Cdc1b. CDC11b transcription is developmentally regulated, producing different amounts of Cdc11a- and Cdc11b-complexes in the lifecycle of Ashbya gossypii. Deletion of either gene results in distinct cell polarity defects, suggesting non-overlapping functions. Cdc11a and Cdc11b complexes have differences in filament length and membrane-binding ability. Thus, septin subunit composition has functional consequences on filament properties and cell morphogenesis. Small sequence differences elicit distinct biophysical properties and cell functions of septins, illuminating how gene duplication could be a driving force for septin gene expansions seen throughout the tree of life. Rockefeller University Press 2023-02-14 /pmc/articles/PMC9960279/ /pubmed/36786832 http://dx.doi.org/10.1083/jcb.202204063 Text en © 2023 Cannon et al. https://creativecommons.org/licenses/by-nc-sa/4.0/http://www.rupress.org/terms/This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Article Cannon, Kevin S. Vargas-Muniz, Jose M. Billington, Neil Seim, Ian Ekena, Joanne Sellers, James R. Gladfelter, Amy. S. A gene duplication of a septin reveals a developmentally regulated filament length control mechanism |
title | A gene duplication of a septin reveals a developmentally regulated filament length control mechanism |
title_full | A gene duplication of a septin reveals a developmentally regulated filament length control mechanism |
title_fullStr | A gene duplication of a septin reveals a developmentally regulated filament length control mechanism |
title_full_unstemmed | A gene duplication of a septin reveals a developmentally regulated filament length control mechanism |
title_short | A gene duplication of a septin reveals a developmentally regulated filament length control mechanism |
title_sort | gene duplication of a septin reveals a developmentally regulated filament length control mechanism |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9960279/ https://www.ncbi.nlm.nih.gov/pubmed/36786832 http://dx.doi.org/10.1083/jcb.202204063 |
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