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dc.contributor.authorMcJunkin, Katherine
dc.contributor.authorAmbros, Victor R.
dc.date2022-08-11T08:10:18.000
dc.date.accessioned2022-08-23T17:03:27Z
dc.date.available2022-08-23T17:03:27Z
dc.date.issued2014-07-21
dc.date.submitted2015-01-12
dc.identifier.citationG3 (Bethesda). 2014 Jul 21;4(9):1747-54. doi: 10.1534/g3.114.011973. <a href="http://dx.doi.org/10.1534/g3.114.011973">Link to article on publisher's site</a>
dc.identifier.issn2160-1836 (Linking)
dc.identifier.doi10.1534/g3.114.011973
dc.identifier.pmid25053708
dc.identifier.urihttp://hdl.handle.net/20.500.14038/44428
dc.description.abstractMicroRNAs guide many aspects of development in all metazoan species. Frequently, microRNAs are expressed during a specific developmental stage to perform a temporally defined function. The C. elegans mir-35-42 microRNAs are expressed abundantly in oocytes and early embryos and are essential for embryonic development. Here, we show that these embryonic microRNAs surprisingly also function to control the number of progeny produced by adult hermaphrodites. Using a temperature-sensitive mir-35-42 family mutant (a deletion of the mir-35-41 cluster), we demonstrate three distinct defects in hermaphrodite fecundity. At permissive temperatures, a mild sperm defect partially reduces hermaphrodite fecundity. At restrictive temperatures, somatic gonad dysfunction combined with a severe sperm defect sharply reduces fecundity. Multiple lines of evidence, including a late embryonic temperature-sensitive period, support a role for mir-35-41 early during development to promote subsequent sperm production in later larval stages. We further show that the predicted mir-35 family target sup-26 (suppressor-26) acts downstream of mir-35-41 in this process, suggesting that sup-26 de-repression in mir-35-41 deletion mutants may contribute to temperature-sensitive loss of fecundity. In addition, these microRNAs play a role in male fertility, promoting proper morphogenesis of male-specific mating structures. Overall, our results demonstrate that robust activity of the mir-35-42 family microRNAs not only is essential for embryonic development across a range of temperatures but also enables the worm to subsequently develop full reproductive capacity.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=25053708&dopt=Abstract">Link to Article in PubMed</a>
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/
dc.subjectfertility
dc.subjectgermline
dc.subjectmale fertility
dc.subjectmaternal effect
dc.subjectsperm
dc.subjectBiochemistry
dc.subjectDevelopmental Biology
dc.subjectMolecular Biology
dc.subjectMolecular Genetics
dc.titleThe embryonic mir-35 family of microRNAs promotes multiple aspects of fecundity in Caenorhabditis elegans
dc.typeJournal Article
dc.source.journaltitleG3 (Bethesda, Md.)
dc.source.volume4
dc.source.issue9
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1019&amp;context=pmm_pp&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/pmm_pp/20
dc.identifier.contextkey6519772
refterms.dateFOA2022-08-23T17:03:27Z
html.description.abstract<p>MicroRNAs guide many aspects of development in all metazoan species. Frequently, microRNAs are expressed during a specific developmental stage to perform a temporally defined function. The C. elegans mir-35-42 microRNAs are expressed abundantly in oocytes and early embryos and are essential for embryonic development. Here, we show that these embryonic microRNAs surprisingly also function to control the number of progeny produced by adult hermaphrodites. Using a temperature-sensitive mir-35-42 family mutant (a deletion of the mir-35-41 cluster), we demonstrate three distinct defects in hermaphrodite fecundity. At permissive temperatures, a mild sperm defect partially reduces hermaphrodite fecundity. At restrictive temperatures, somatic gonad dysfunction combined with a severe sperm defect sharply reduces fecundity. Multiple lines of evidence, including a late embryonic temperature-sensitive period, support a role for mir-35-41 early during development to promote subsequent sperm production in later larval stages. We further show that the predicted mir-35 family target sup-26 (suppressor-26) acts downstream of mir-35-41 in this process, suggesting that sup-26 de-repression in mir-35-41 deletion mutants may contribute to temperature-sensitive loss of fecundity. In addition, these microRNAs play a role in male fertility, promoting proper morphogenesis of male-specific mating structures. Overall, our results demonstrate that robust activity of the mir-35-42 family microRNAs not only is essential for embryonic development across a range of temperatures but also enables the worm to subsequently develop full reproductive capacity.</p>
dc.identifier.submissionpathpmm_pp/20
dc.contributor.departmentRNA Therapeutics Institute
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pages1747-54


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