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dc.contributor.authorTran, Christina
dc.date.accessioned2016-06-24T16:35:07Z
dc.date.available2016-06-24T16:35:07Z
dc.date.issued2016-01-25
dc.identifier.urihttp://hdl.handle.net/1808/21021
dc.descriptionThis undergraduate research project is being made available in KU ScholarWorks with the permission of the author. The project was supervised by Dr. Paulyn Cartwright, associate professor of Ecology and Evolutionary Biology at the University of Kansas.en_US
dc.description.abstractThe sea anemone, Nematostella vectensis, has the ability to fully regenerate amputated body parts. We hypothesize that Runx, a transcription factor, controls the cellular processes for regeneration, specifically the transition between cellular proliferation and cellular differentiation. A known inhibitor to the Runx pathway is Ro5-3335, a benzodiazepine. Inhibiting the Runx pathway by Ro5-3335 will help determine if Runx is necessary for proper regeneration in Nematostella. We introduced bisected Nematostella polyps to Ro5-3335 for a 24-48 period and observed regeneration of oral ends. Tentacle regeneration appeared delayed in treated polyps compared to the controls. It was not until three weeks post-treatment that the treated animals recovered normal regeneration. We conclude that Ro5-3335 appears to repress regeneration in the polyps which suggests that the Runx pathway is important for proper regeneration in Nematostella.en_US
dc.publisherDepartment of Ecology & Evolutionary Biology, University of Kansasen_US
dc.titleInhibition of Runx by Ro5-3335 Affects Nematostella Regenerationen_US
dc.typeUndergraduate research project
dc.thesis.degreeDisciplineEcology and Evolutionary Biology
dc.provenanceThis paper is being made available with the permission of the author and at the request of the sponsoring faculty member. The permission form has been uploaded to this record as a License bitstream. -- Marianne
kusw.oaversionScholarly/refereed, publisher versionen_US
kusw.oapolicyThis item does not meet KU Open Access policy criteria.en_US
dc.rights.accessrightsopenAccess


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