Date Approved
12-2011
Graduate Degree Type
Thesis
Degree Name
Cell and Molecular Biology (M.S.)
Degree Program
Cell and Molecular Biology
Abstract
Sprouty 2 (Spry2), one of the four mammalian Spry family members, is a negative feedback regulator of many receptor tyrosine kinases (RTKs) signaling including Met. It fine-tunes RTKs signaling through multiple levels of regulations starting from RTK itself to several downstream molecules that are crucial for signal transduction. To understand what role Spry2 might play during developmental processes, we created a Spry2 conventional knockout mouse in which Spry2 expression is replaced by enhanced green fluorescent protein (EGFP) reporter. Spry2 appears to be expressed in mouse embryo and in many adult tissues, and Spry2- deficient mice have smaller body size and shorter lifespan. Pathologically, we observed that Spry2 deficiency results in impaired relaxation of the lower esophageal sphincter and mega-esophagus, a condition known as achalasia, which is likely due to malfunction of the innervated neurons where Spry2 is expressed. The Spry2-deficient mice may serve as a useful animal model for achalasia. Currently, we are investigating how loss of Spry2 leads to achalasia and whether the Met pathway plays a role in the development of this phenotype.
ScholarWorks Citation
Staal, Benjamin Lee, "Sprouty2 Deficiency in Mice Leads to the Development of Achalasia" (2011). Masters Theses. 11.
https://scholarworks.gvsu.edu/theses/11
