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dc.contributor.authorSherrard, Ryan
dc.contributor.authorLuehr, Sebastian
dc.contributor.authorHolzkamp, Heinke
dc.contributor.authorMcJunkin, Katherine
dc.contributor.authorMemar, Nadin
dc.contributor.authorConradt, Barbara
dc.date2022-08-11T08:09:47.000
dc.date.accessioned2022-08-23T16:43:20Z
dc.date.available2022-08-23T16:43:20Z
dc.date.issued2017-01-15
dc.date.submitted2017-06-09
dc.identifier.citationGenes Dev. 2017 Jan 15;31(2):209-222. Epub 2017 Feb 6. <a href="https://doi.org/10.1101/gad.288555.116">Link to article on publisher's site</a>
dc.identifier.issn0890-9369 (Linking)
dc.identifier.doi10.1101/gad.288555.116
dc.identifier.pmid28167500
dc.identifier.urihttp://hdl.handle.net/20.500.14038/40270
dc.description.abstractProgrammed cell death occurs in a highly reproducible manner during Caenorhabditis elegans development. We demonstrate that, during embryogenesis, miR-35 and miR-58 bantam family microRNAs (miRNAs) cooperate to prevent the precocious death of mothers of cells programmed to die by repressing the gene egl-1, which encodes a proapoptotic BH3-only protein. In addition, we present evidence that repression of egl-1 is dependent on binding sites for miR-35 and miR-58 family miRNAs within the egl-1 3' untranslated region (UTR), which affect both mRNA copy number and translation. Furthermore, using single-molecule RNA fluorescent in situ hybridization (smRNA FISH), we show that egl-1 is transcribed in the mother of a cell programmed to die and that miR-35 and miR-58 family miRNAs prevent this mother from dying by keeping the copy number of egl-1 mRNA below a critical threshold. Finally, miR-35 and miR-58 family miRNAs can also dampen the transcriptional boost of egl-1 that occurs specifically in a daughter cell that is programmed to die. We propose that miRNAs compensate for lineage-specific differences in egl-1 transcriptional activation, thus ensuring that EGL-1 activity reaches the threshold necessary to trigger death only in daughter cells that are programmed to die.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=28167500&dopt=Abstract">Link to Article in PubMed</a>
dc.rightsCopyright 2017 Sherrard et al. Freely available online through the Genes and Development Open Access option.
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectBH3-only
dc.subjectC. elegans
dc.subjectdevelopment
dc.subjectembryo
dc.subjectmiRNA
dc.subjectprogrammed cell death
dc.subjectCell Biology
dc.subjectDevelopmental Biology
dc.titlemiRNAs cooperate in apoptosis regulation during C. elegans development
dc.typeJournal Article
dc.source.journaltitleGenes and development
dc.source.volume31
dc.source.issue2
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=4070&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/3065
dc.identifier.contextkey10275040
refterms.dateFOA2022-08-23T16:43:20Z
html.description.abstract<p>Programmed cell death occurs in a highly reproducible manner during Caenorhabditis elegans development. We demonstrate that, during embryogenesis, miR-35 and miR-58 bantam family microRNAs (miRNAs) cooperate to prevent the precocious death of mothers of cells programmed to die by repressing the gene egl-1, which encodes a proapoptotic BH3-only protein. In addition, we present evidence that repression of egl-1 is dependent on binding sites for miR-35 and miR-58 family miRNAs within the egl-1 3' untranslated region (UTR), which affect both mRNA copy number and translation. Furthermore, using single-molecule RNA fluorescent in situ hybridization (smRNA FISH), we show that egl-1 is transcribed in the mother of a cell programmed to die and that miR-35 and miR-58 family miRNAs prevent this mother from dying by keeping the copy number of egl-1 mRNA below a critical threshold. Finally, miR-35 and miR-58 family miRNAs can also dampen the transcriptional boost of egl-1 that occurs specifically in a daughter cell that is programmed to die. We propose that miRNAs compensate for lineage-specific differences in egl-1 transcriptional activation, thus ensuring that EGL-1 activity reaches the threshold necessary to trigger death only in daughter cells that are programmed to die.</p>
dc.identifier.submissionpathoapubs/3065
dc.contributor.departmentRNA Therapeutics Institute
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pages209-222


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Copyright 2017 Sherrard et al. Freely available online through the Genes and Development Open Access option.
Except where otherwise noted, this item's license is described as Copyright 2017 Sherrard et al. Freely available online through the Genes and Development Open Access option.