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dc.contributor.authorLee, Yongchan
dc.contributor.authorHamann, Jens C.
dc.contributor.authorPellegrino, Mark
dc.contributor.authorDurgan, Joanne
dc.contributor.authorDomart, Marie-Charlotte
dc.contributor.authorCollinson, Lucy M.
dc.contributor.authorHaynes, Cole M.
dc.contributor.authorFlorey, Oliver
dc.contributor.authorOverholtzer, Michael
dc.date2022-08-11T08:09:52.000
dc.date.accessioned2022-08-23T16:46:59Z
dc.date.available2022-08-23T16:46:59Z
dc.date.issued2019-03-19
dc.date.submitted2019-05-16
dc.identifier.citation<p>Cell Rep. 2019 Mar 19;26(12):3212-3220.e4. doi: 10.1016/j.celrep.2019.02.073. <a href="https://doi.org/10.1016/j.celrep.2019.02.073">Link to article on publisher's site</a></p>
dc.identifier.issn2211-1247 (Electronic)
dc.identifier.doi10.1016/j.celrep.2019.02.073
dc.identifier.pmid30893595
dc.identifier.urihttp://hdl.handle.net/20.500.14038/40990
dc.description.abstractMetazoan cell death mechanisms are diverse and include numerous non-apoptotic programs. One program called entosis involves the invasion of live cells into their neighbors and is known to occur in cancers. Here, we identify a developmental function for entosis: to clear the male-specific linker cell in C. elegans. The linker cell leads migration to shape the gonad and is removed to facilitate fusion of the gonad to the cloaca. We find that the linker cell is cleared in a manner involving cell-cell adhesions and cell-autonomous control of uptake through linker cell actin. Linker cell entosis generates a lobe structure that is deposited at the site of gonad-to-cloaca fusion and is removed during mating. Inhibition of lobe scission inhibits linker cell death, demonstrating that the linker cell invades its host while alive. Our findings demonstrate a developmental function for entosis: to eliminate a migrating cell and facilitate gonad-to-cloaca fusion, which is required for fertility.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=30893595&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rightsCopyright 2019 The Authors. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectcell adhesion
dc.subjectcell cannibalism
dc.subjectengulfment
dc.subjectentosis
dc.subjectentotic cell death
dc.subjectgonad
dc.subjectlinker cell death
dc.subjectlobe
dc.subjectscission
dc.subjecturopod
dc.subjectCell Biology
dc.subjectCells
dc.subjectDevelopmental Biology
dc.subjectEmbryonic Structures
dc.titleEntosis Controls a Developmental Cell Clearance in C. elegans
dc.typeJournal Article
dc.source.journaltitleCell reports
dc.source.volume26
dc.source.issue12
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=4801&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/3787
dc.identifier.contextkey14516627
refterms.dateFOA2022-08-23T16:46:59Z
html.description.abstract<p>Metazoan cell death mechanisms are diverse and include numerous non-apoptotic programs. One program called entosis involves the invasion of live cells into their neighbors and is known to occur in cancers. Here, we identify a developmental function for entosis: to clear the male-specific linker cell in C. elegans. The linker cell leads migration to shape the gonad and is removed to facilitate fusion of the gonad to the cloaca. We find that the linker cell is cleared in a manner involving cell-cell adhesions and cell-autonomous control of uptake through linker cell actin. Linker cell entosis generates a lobe structure that is deposited at the site of gonad-to-cloaca fusion and is removed during mating. Inhibition of lobe scission inhibits linker cell death, demonstrating that the linker cell invades its host while alive. Our findings demonstrate a developmental function for entosis: to eliminate a migrating cell and facilitate gonad-to-cloaca fusion, which is required for fertility.</p>
dc.identifier.submissionpathoapubs/3787
dc.contributor.departmentDepartment of Molecular, Cell and Cancer Biology
dc.source.pages3212-3220.e4


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Copyright 2019 The Authors. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Except where otherwise noted, this item's license is described as Copyright 2019 The Authors. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).