A gene duplication of a septin reveals a developmentally regulated filament length control mechanism

dc.contributor.author Cannon, Kevin S
dc.contributor.author Vargas-Muniz, Jose M.
dc.contributor.author Billington, Neil
dc.contributor.author Seim, Ian
dc.contributor.author Ekena, Joanne
dc.contributor.author Sellers, James R.
dc.contributor.author Gladfelter, Amy S.
dc.date.accessioned 2023-09-26T20:44:29Z
dc.date.available 2023-09-26T20:44:29Z
dc.date.issued 2023-02-14
dc.description © The Author(s), 2023. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Cannon, K., Vargas-Muniz, J., Billington, N., Seim, I., Ekena, J., Sellers, J., & Gladfelter, A. A gene duplication of a septin reveals a developmentally regulated filament length control mechanism. Journal of Cell Biology, 222(3), (2023): e202204063, https://doi.org/10.1083/jcb.202204063.
dc.description.abstract 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.
dc.description.sponsorship This work was supported by National Science Foundation MCB-1615138 and MCB-2016022, and a Howard Hughes Medical Institute Faculty Scholars award to A.S. Gladfelter. K.S. Cannon was supported in part by a grant from the National Institute of General Medical Sciences under award T32 GM 119999. J.M. Vargas-Muniz was supported by National Institutes of Health Training Grant 5T32AI052080-14.
dc.identifier.citation Cannon, K., Vargas-Muniz, J., Billington, N., Seim, I., Ekena, J., Sellers, J., & Gladfelter, A. (2023). A gene duplication of a septin reveals a developmentally regulated filament length control mechanism. Journal of Cell Biology, 222(3), e202204063.
dc.identifier.doi 10.1083/jcb.202204063
dc.identifier.uri https://hdl.handle.net/1912/66898
dc.publisher Rockefeller University Press
dc.relation.uri https://doi.org/10.1083/jcb.202204063
dc.rights Attribution-NonCommercial-ShareAlike 4.0 International *
dc.rights.uri http://creativecommons.org/licenses/by-nc-sa/4.0/ *
dc.title A gene duplication of a septin reveals a developmentally regulated filament length control mechanism
dc.type Article
dspace.entity.type Publication
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