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Drosophila septin interacting protein 1 regulates neurogenesis in the early developing larval brain
Neurogenesis in the Drosophila central brain progresses dynamically in order to generate appropriate numbers of neurons during different stages of development. Thus, a central challenge in neurobiology is to reveal the molecular and genetic mechanisms of neurogenesis timing. Here, we found that neur...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8742078/ https://www.ncbi.nlm.nih.gov/pubmed/34997175 http://dx.doi.org/10.1038/s41598-021-04474-3 |
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author | Wei, Jia-Yi Chu, Sao-Yu Huang, Yu-Chien Chung, Pei-Chi Yu, Hung-Hsiang |
author_facet | Wei, Jia-Yi Chu, Sao-Yu Huang, Yu-Chien Chung, Pei-Chi Yu, Hung-Hsiang |
author_sort | Wei, Jia-Yi |
collection | PubMed |
description | Neurogenesis in the Drosophila central brain progresses dynamically in order to generate appropriate numbers of neurons during different stages of development. Thus, a central challenge in neurobiology is to reveal the molecular and genetic mechanisms of neurogenesis timing. Here, we found that neurogenesis is significantly impaired when a novel mutation, Nuwa, is induced at early but not late larval stages. Intriguingly, when the Nuwa mutation is induced in neuroblasts of olfactory projection neurons (PNs) at the embryonic stage, embryonic-born PNs are generated, but larval-born PNs of the same origin fail to be produced. Through molecular characterization and transgenic rescue experiments, we determined that Nuwa is a loss-of-function mutation in Drosophila septin interacting protein 1 (sip1). Furthermore, we found that SIP1 expression is enriched in neuroblasts, and RNAi knockdown of sip1 using a neuroblast driver results in formation of small and aberrant brains. Finally, full-length SIP1 protein and truncated SIP1 proteins lacking either the N- or C-terminus display different subcellular localization patterns, and only full-length SIP1 can rescue the Nuwa-associated neurogenesis defect. Taken together, these results suggest that SIP1 acts as a crucial factor for specific neurogenesis programs in the early developing larval brain. |
format | Online Article Text |
id | pubmed-8742078 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-87420782022-01-11 Drosophila septin interacting protein 1 regulates neurogenesis in the early developing larval brain Wei, Jia-Yi Chu, Sao-Yu Huang, Yu-Chien Chung, Pei-Chi Yu, Hung-Hsiang Sci Rep Article Neurogenesis in the Drosophila central brain progresses dynamically in order to generate appropriate numbers of neurons during different stages of development. Thus, a central challenge in neurobiology is to reveal the molecular and genetic mechanisms of neurogenesis timing. Here, we found that neurogenesis is significantly impaired when a novel mutation, Nuwa, is induced at early but not late larval stages. Intriguingly, when the Nuwa mutation is induced in neuroblasts of olfactory projection neurons (PNs) at the embryonic stage, embryonic-born PNs are generated, but larval-born PNs of the same origin fail to be produced. Through molecular characterization and transgenic rescue experiments, we determined that Nuwa is a loss-of-function mutation in Drosophila septin interacting protein 1 (sip1). Furthermore, we found that SIP1 expression is enriched in neuroblasts, and RNAi knockdown of sip1 using a neuroblast driver results in formation of small and aberrant brains. Finally, full-length SIP1 protein and truncated SIP1 proteins lacking either the N- or C-terminus display different subcellular localization patterns, and only full-length SIP1 can rescue the Nuwa-associated neurogenesis defect. Taken together, these results suggest that SIP1 acts as a crucial factor for specific neurogenesis programs in the early developing larval brain. Nature Publishing Group UK 2022-01-07 /pmc/articles/PMC8742078/ /pubmed/34997175 http://dx.doi.org/10.1038/s41598-021-04474-3 Text en © The Author(s) 2022 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 Wei, Jia-Yi Chu, Sao-Yu Huang, Yu-Chien Chung, Pei-Chi Yu, Hung-Hsiang Drosophila septin interacting protein 1 regulates neurogenesis in the early developing larval brain |
title | Drosophila septin interacting protein 1 regulates neurogenesis in the early developing larval brain |
title_full | Drosophila septin interacting protein 1 regulates neurogenesis in the early developing larval brain |
title_fullStr | Drosophila septin interacting protein 1 regulates neurogenesis in the early developing larval brain |
title_full_unstemmed | Drosophila septin interacting protein 1 regulates neurogenesis in the early developing larval brain |
title_short | Drosophila septin interacting protein 1 regulates neurogenesis in the early developing larval brain |
title_sort | drosophila septin interacting protein 1 regulates neurogenesis in the early developing larval brain |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8742078/ https://www.ncbi.nlm.nih.gov/pubmed/34997175 http://dx.doi.org/10.1038/s41598-021-04474-3 |
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