The Drosophila midgut is an outstanding model system to study the basis of homeostatic control in animals due to its simplified set of cell types, which includes highly similar cell types to those in the mammalian intestine. When damaged or aged cells are lost from the epithelium of the Drosophila midgut, ISCs respond to this stress and maintain gut homeostasis by dividing to replenish the intestinal epithelium. During this response, the epidermal growth factor (EGFR)/Ras/MAPK signaling pathway is induced in ISCs, which promotes ISC division and midgut epithelium regeneration.Capicua (Cic), an HMG-box transcriptional repressor was shown to be a key regulator of cell proliferation and differentiation downstream of receptor tyrosine kinase/Ras signaling pathway in Drosophila embryos, wings and eyes. It also has a C2 motif which functions as a MAPK docking site responsible for down-regulation of Cic by Torso and EGFR RTK signaling. Therefore, Cic is hypothesized to be a repressor that acts downstream of EGFR signaling to maintain normal ISC proliferation. However, whether Cic does indeed act as downstream of the EGFR signaling pathway to regulate ISC proliferation is yet unknown. Furthermore, the underlying mechanisms by which Cic controls ISC proliferation also need to be defined. Hence, in this project, we would like to understand how Cic is regulated by the EGFR signaling, and how it in turn regulates ISC proliferation.