Research interests
Genetically altered cells frequently arise in epithelial tissues due to developmental errors or mutagenesis. Maintaining tissue homeostasis and organismal health requires recognition and elimination of such aberrant cells through tissue-intrinsic error corrections mechanisms. One such mechanism, interface surveillance (IS), ensures the removal of cells with mutations in signaling pathways or cell-fate regulators. My PhD project aims to determine how differential expression levels of Robo2 translate into mechanical and signaling asymmetries to activate IS. Understanding these processes provides critical insights into how cell-surface molecule heterogeneity ensures tissue integrity through interface surveillance.
