Show simple item record

dc.contributor.authorNie, Yingchao
dc.contributor.authorLi, Qi
dc.contributor.authorAmcheslavsky, Alla
dc.contributor.authorDuhart, Juan Carlos
dc.contributor.authorVeraksa, Alexey
dc.contributor.authorStocker, Hugo
dc.contributor.authorRaftery, Laurel A.
dc.contributor.authorIp, Y. Tony
dc.date2022-08-11T08:09:44.000
dc.date.accessioned2022-08-23T16:41:19Z
dc.date.available2022-08-23T16:41:19Z
dc.date.issued2015-12-01
dc.date.submitted2015-12-23
dc.identifier.citationStem Cell Rev. 2015 Dec;11(6):813-25. doi: 10.1007/s12015-015-9617-5. <a href="http://dx.doi.org/10.1007/s12015-015-9617-5">Link to article on publisher's site</a>
dc.identifier.issn1550-8943 (Linking)
dc.identifier.doi10.1007/s12015-015-9617-5
dc.identifier.pmid26323255
dc.identifier.urihttp://hdl.handle.net/20.500.14038/39858
dc.description.abstractThe Drosophila adult midgut contains intestinal stem cells that support homeostasis and repair. We show here that the leucine zipper protein Bunched and the adaptor protein Madm are novel regulators of intestinal stem cells. MARCM mutant clonal analysis and cell type specific RNAi revealed that Bunched and Madm were required within intestinal stem cells for proliferation. Transgenic expression of a tagged Bunched showed a cytoplasmic localization in midgut precursors, and the addition of a nuclear localization signal to Bunched reduced its function to cooperate with Madm to increase intestinal stem cell proliferation. Furthermore, the elevated cell growth and 4EBP phosphorylation phenotypes induced by loss of Tuberous Sclerosis Complex or overexpression of Rheb were suppressed by the loss of Bunched or Madm. Therefore, while the mammalian homolog of Bunched, TSC-22, is able to regulate transcription and suppress cancer cell proliferation, our data suggest the model that Bunched and Madm functionally interact with the TOR pathway in the cytoplasm to regulate the growth and subsequent division of intestinal stem cells.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=26323255&dopt=Abstract">Link to Article in PubMed</a>
dc.rights<p>This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/ licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.</p>
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectUMCCTS funding
dc.subjectBunched
dc.subjectDrosophila
dc.subjectIntestine
dc.subjectMadm
dc.subjectStem cells
dc.subjectTSC-22
dc.subjectTuberous sclerosis complex
dc.subjectCell Biology
dc.titleBunched and Madm Function Downstream of Tuberous Sclerosis Complex to Regulate the Growth of Intestinal Stem Cells in Drosophila
dc.typeJournal Article
dc.source.journaltitleStem cell reviews
dc.source.volume11
dc.source.issue6
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=3660&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/2656
dc.identifier.contextkey7972038
refterms.dateFOA2022-08-23T16:41:19Z
html.description.abstract<p>The Drosophila adult midgut contains intestinal stem cells that support homeostasis and repair. We show here that the leucine zipper protein Bunched and the adaptor protein Madm are novel regulators of intestinal stem cells. MARCM mutant clonal analysis and cell type specific RNAi revealed that Bunched and Madm were required within intestinal stem cells for proliferation. Transgenic expression of a tagged Bunched showed a cytoplasmic localization in midgut precursors, and the addition of a nuclear localization signal to Bunched reduced its function to cooperate with Madm to increase intestinal stem cell proliferation. Furthermore, the elevated cell growth and 4EBP phosphorylation phenotypes induced by loss of Tuberous Sclerosis Complex or overexpression of Rheb were suppressed by the loss of Bunched or Madm. Therefore, while the mammalian homolog of Bunched, TSC-22, is able to regulate transcription and suppress cancer cell proliferation, our data suggest the model that Bunched and Madm functionally interact with the TOR pathway in the cytoplasm to regulate the growth and subsequent division of intestinal stem cells.</p>
dc.identifier.submissionpathoapubs/2656
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pages813-25


Files in this item

Thumbnail
Name:
art_3A10.1007_2Fs12015_015_961 ...
Size:
1.774Mb
Format:
PDF

This item appears in the following Collection(s)

Show simple item record

<p>This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/ licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.</p>
Except where otherwise noted, this item's license is described as <p>This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/ licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.</p>