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The endoplasmic reticulum is partitioned asymmetrically during mitosis before cell fate selection in proneuronal cells in the early Drosophila embryo
Asymmetric cell division is the primary mechanism to generate cellular diversity, and it relies on the correct partitioning of cell fate determinants. However, the mechanism by which these determinants are delivered and positioned is poorly understood, and the upstream signal to initiate asymmetric...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The American Society for Cell Biology
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5449151/ https://www.ncbi.nlm.nih.gov/pubmed/28381427 http://dx.doi.org/10.1091/mbc.E16-09-0690 |
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author | Eritano, Anthony S. Altamirano, Arturo Beyeler, Sarah Gaytan, Norma Velasquez, Mark Riggs, Blake |
author_facet | Eritano, Anthony S. Altamirano, Arturo Beyeler, Sarah Gaytan, Norma Velasquez, Mark Riggs, Blake |
author_sort | Eritano, Anthony S. |
collection | PubMed |
description | Asymmetric cell division is the primary mechanism to generate cellular diversity, and it relies on the correct partitioning of cell fate determinants. However, the mechanism by which these determinants are delivered and positioned is poorly understood, and the upstream signal to initiate asymmetric cell division is unknown. Here we report that the endoplasmic reticulum (ER) is asymmetrically partitioned during mitosis in epithelial cells just before delamination and selection of a proneural cell fate in the early Drosophila embryo. At the start of gastrulation, the ER divides asymmetrically into a population of asynchronously dividing cells at the anterior end of the embryo. We found that this asymmetric division of the ER depends on the highly conserved ER membrane protein Jagunal (Jagn). RNA inhibition of jagn just before the start of gastrulation disrupts this asymmetric division of the ER. In addition, jagn-deficient embryos display defects in apical-basal spindle orientation in delaminated embryonic neuroblasts. Our results describe a model in which an organelle is partitioned asymmetrically in an otherwise symmetrically dividing cell population just upstream of cell fate determination and updates previous models of spindle-based selection of cell fate during mitosis. |
format | Online Article Text |
id | pubmed-5449151 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | The American Society for Cell Biology |
record_format | MEDLINE/PubMed |
spelling | pubmed-54491512017-08-16 The endoplasmic reticulum is partitioned asymmetrically during mitosis before cell fate selection in proneuronal cells in the early Drosophila embryo Eritano, Anthony S. Altamirano, Arturo Beyeler, Sarah Gaytan, Norma Velasquez, Mark Riggs, Blake Mol Biol Cell Articles Asymmetric cell division is the primary mechanism to generate cellular diversity, and it relies on the correct partitioning of cell fate determinants. However, the mechanism by which these determinants are delivered and positioned is poorly understood, and the upstream signal to initiate asymmetric cell division is unknown. Here we report that the endoplasmic reticulum (ER) is asymmetrically partitioned during mitosis in epithelial cells just before delamination and selection of a proneural cell fate in the early Drosophila embryo. At the start of gastrulation, the ER divides asymmetrically into a population of asynchronously dividing cells at the anterior end of the embryo. We found that this asymmetric division of the ER depends on the highly conserved ER membrane protein Jagunal (Jagn). RNA inhibition of jagn just before the start of gastrulation disrupts this asymmetric division of the ER. In addition, jagn-deficient embryos display defects in apical-basal spindle orientation in delaminated embryonic neuroblasts. Our results describe a model in which an organelle is partitioned asymmetrically in an otherwise symmetrically dividing cell population just upstream of cell fate determination and updates previous models of spindle-based selection of cell fate during mitosis. The American Society for Cell Biology 2017-06-01 /pmc/articles/PMC5449151/ /pubmed/28381427 http://dx.doi.org/10.1091/mbc.E16-09-0690 Text en © 2017 Eritano et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0). “ASCB®,” “The American Society for Cell Biology®,” and “Molecular Biology of the Cell®” are registered trademarks of The American Society for Cell Biology. |
spellingShingle | Articles Eritano, Anthony S. Altamirano, Arturo Beyeler, Sarah Gaytan, Norma Velasquez, Mark Riggs, Blake The endoplasmic reticulum is partitioned asymmetrically during mitosis before cell fate selection in proneuronal cells in the early Drosophila embryo |
title | The endoplasmic reticulum is partitioned asymmetrically during mitosis before cell fate selection in proneuronal cells in the early Drosophila embryo |
title_full | The endoplasmic reticulum is partitioned asymmetrically during mitosis before cell fate selection in proneuronal cells in the early Drosophila embryo |
title_fullStr | The endoplasmic reticulum is partitioned asymmetrically during mitosis before cell fate selection in proneuronal cells in the early Drosophila embryo |
title_full_unstemmed | The endoplasmic reticulum is partitioned asymmetrically during mitosis before cell fate selection in proneuronal cells in the early Drosophila embryo |
title_short | The endoplasmic reticulum is partitioned asymmetrically during mitosis before cell fate selection in proneuronal cells in the early Drosophila embryo |
title_sort | endoplasmic reticulum is partitioned asymmetrically during mitosis before cell fate selection in proneuronal cells in the early drosophila embryo |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5449151/ https://www.ncbi.nlm.nih.gov/pubmed/28381427 http://dx.doi.org/10.1091/mbc.E16-09-0690 |
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