Rab11 Is Required for Epithelial Cell Viability, Terminal Differentiation, and Suppression of Tumor-Like Growth in the Drosophila Egg Chamber
dc.contributor.author | Xu, Jiang | |
dc.contributor.author | Lan, Lan | |
dc.contributor.author | Bogard, Nicholas | |
dc.contributor.author | Mattione, Cristin | |
dc.contributor.author | Cohen, Robert S. | |
dc.date.accessioned | 2014-03-14T19:25:37Z | |
dc.date.available | 2014-03-14T19:25:37Z | |
dc.date.issued | 2011-05-23 | |
dc.identifier.citation | Xu, J., Lan, L., Bogard, N., Mattione, C., & Cohen, R. S. (2011). Rab11 Is Required for Epithelial Cell Viability, Terminal Differentiation, and Suppression of Tumor-Like Growth in the Drosophila Egg Chamber. PLoS ONE, 6(5). http://dx.doi.org/10.1371/journal.pone.0020180 | |
dc.identifier.uri | http://hdl.handle.net/1808/13172 | |
dc.description.abstract | Background: The Drosophila egg chamber provides an excellent system in which to study the specification and differentiation of epithelial cell fates because all of the steps, starting with the division of the corresponding stem cells, called follicle stem cells, have been well described and occur many times over in a single ovary.Methodology/Principal Findings: Here we investigate the role of the small Rab11 GTPase in follicle stem cells (FSCs) and in their differentiating daughters, which include main body epithelial cells, stalk cells and polar cells. We show that rab11-null FSCs maintain their ability to self renew, even though previous studies have shown that FSC self renewal is dependent on maintenance of E-cadherin-based intercellular junctions, which in many cell types, including Drosophila germline stem cells, requires Rab11. We also show that rab11-null FSCs give rise to normal numbers of cells that enter polar, stalk, and epithelial cell differentiation pathways, but that none of the cells complete their differentiation programs and that the epithelial cells undergo premature programmed cell death. Finally we show, through the induction of rab11-null clones at later points in the differentiation program, that Rab11 suppresses tumor-like growth of epithelial cells. Thus, rab11-null epithelial cells arrest differentiation early, assume an aberrant cell morphology, delaminate from the epithelium, and invade the neighboring germline cyst. These phenotypes are associated with defects in E-cadherin localization and a general loss of cell polarity.Conclusions/Significance: While previous studies have revealed tumor suppressor or tumor suppressor-like activity for regulators of endocytosis, our study is the first to identify such activity for regulators of endocytic recycling. Our studies also support the recently emerging view that distinct mechanisms regulate junction stability and plasticity in different tissues. | |
dc.description.sponsorship | Funding: This work was supported by National Institutes of Health Grants P20 RR15563 and R01 GM068022. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. | |
dc.publisher | Public Library of Science | |
dc.rights | Copyright: ©2011 Xu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. | |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | |
dc.subject | Cell cycle and cell division | |
dc.subject | Cell differentiation | |
dc.subject | Cell polarity | |
dc.subject | Cell staining | |
dc.subject | Drosophila melanogaster | |
dc.subject | Epithelial Cells | |
dc.subject | Epithelium | |
dc.subject | Oocytes | |
dc.title | Rab11 Is Required for Epithelial Cell Viability, Terminal Differentiation, and Suppression of Tumor-Like Growth in the Drosophila Egg Chamber | |
dc.type | Article | |
kusw.kuauthor | Xu, Jiang | |
kusw.kuauthor | Lan, Lan | |
kusw.kuauthor | Bogard, Nicholas | |
kusw.kuauthor | Mattione, Cristin | |
kusw.kuauthor | Cohen, Robert S. | |
kusw.kudepartment | Molecular Biosciences | |
kusw.oastatus | fullparticipation | |
dc.identifier.doi | 10.1371/journal.pone.0020180 | |
dc.identifier.orcid | https://orcid.org/0000-0002-6933-5453 | |
kusw.oaversion | Scholarly/refereed, publisher version | |
kusw.oapolicy | This item meets KU Open Access policy criteria. | |
dc.rights.accessrights | openAccess |
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Except where otherwise noted, this item's license is described as: Copyright: ©2011 Xu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.