Presenter(s)
Jessica L. Beebe
Files
Download Project (995 KB)
Description
After injury humans produce scar tissue as part of the wound healing process. This process does not generate new tissue, but prevent the remaining tissue from further damage. Without the ability to create new tissue, humans are limited in their capacity to regain lost function after severe injury. However, axolotls have the ability to regenerate a variety of organs within the first two weeks of hatching, allowing for complete recovery of tissue function. Specifically lens regeneration is studied due to the dynamic changes that occur in the surrounding iris tissue following lens removal. Dorsal and ventral iris cells proliferate and eventually regenerate the missing lens. Since axolotls are not able to regenerate the lens succeeding two weeks from hatching, this is the control group representing non-regenerating tissue. These axolotls contain the same genes which allows for specific manipulation of iris tissues and examination of the different outcomes in hope of revealing the cause of regeneration. The goal of the current project is to study tissue regeneration at the molecular level, by influencing target genes through drug treatments within a specific biological pathway, in order to gain further insight about the mechanism of regeneration. When the mechanism of tissue regeneration is entirely understood, this research could be used to provide treatment in humans with severe tissue damage.
Publication Date
4-9-2015
Project Designation
Honors Thesis
Primary Advisor
Panagiotis A. Tsonis
Primary Advisor's Department
Biology
Keywords
Stander Symposium project
Disciplines
Arts and Humanities | Business | Education | Engineering | Life Sciences | Medicine and Health Sciences | Physical Sciences and Mathematics | Social and Behavioral Sciences
Recommended Citation
"Manipulation of the Wnt Signaling Pathway and Analysis of Gene Expression in Axolotls" (2015). Stander Symposium Projects. 590.
https://ecommons.udayton.edu/stander_posters/590
Included in
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