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dc.contributor.advisorLee, Myeongwoo.
dc.contributor.authorThogmartin, Amanda K.
dc.contributor.otherBaylor University. Dept. of Biology.en
dc.date.accessioned2010-06-23T12:33:54Z
dc.date.available2010-06-23T12:33:54Z
dc.date.copyright2010-05
dc.date.issued2010-06-23T12:33:54Z
dc.identifier.urihttp://hdl.handle.net/2104/7977
dc.descriptionIncludes bibliographical references (p. ).en
dc.description.abstractC. elegans provides a useful system with which to study signaling pathways, giving information that can be applied to many organisms. The use of RNA interference can be used to study the genes involved in many different pathways, including the inositol triphosphate (IP3) signaling pathway. This pathway is involved in maintaining contractions necessary for C. elegans ovulation. Using an RNAi feeding protocol, expression of several protein synthesis and cell signaling genes were knocked down, causing sterility in the wild-type worm. Sterility was rescued in mutants having a constitutively active IP3 receptor (itr-1 (sy290)), revealing that the genes were somehow involved in IP3 signaling. Use of worms with mutant backgrounds of ipp-5 and lfe-2, which are involved in negatively regulating IP3, showed that lfe-2 expression is solely in the spermatheca. When RNAi of ribosomal genes is performed in this mutant, sterility is able to be rescued.en
dc.description.statementofresponsibilityby Amanda K. Thogmartin.en
dc.format.extent2114292 bytes
dc.format.extent675965 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypeapplication/pdf
dc.language.isoen_USen
dc.rightsBaylor University theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission. Contact librarywebmaster@baylor.edu for inquiries about permission.en
dc.subjectCaenorhabditis elegans.en
dc.titleInvestigation of the role of ipp-5 and lfe-2 in the IP3 signaling pathway in Caenorhabditis elegans ovulation.en
dc.typeThesisen
dc.description.degreeM.S.en
dc.rights.accessrightsWorldwide access.en
dc.rights.accessrightsAccess changed 3/18/13.
dc.contributor.departmentBiology.en


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