SIN3 is an important, co-transcriptional repressor that regulates gene transcription. SIN3 is the scaffold protein of the SIN3/HDAC complex, that removes acetyl groups from histone proteins. SIN3 is essential for progression through the cell cycle, cell viability, and supporting energy production in cells. Previous studies conducted in Drosophila used RNA interference (RNAi) mechanism to knock down Sin3A to examine regulated genes. This technique, however, has a few drawbacks, mainly that the reduction in protein expression is incomplete. We aim to develop a new tool to rapidly deplete SIN3 from the nucleus and export it to the cytoplasm. We will use CRISPR-Cas9-mediated homology directed repair to add the light-inducible nuclear export system (LEXY) at the C-terminus of one of the SIN3 isoforms in Drosophila, SIN3 187. Drosophila express different versions of SIN3, called isoforms, which have some unique functions. As a part of developing this tool, I created two guide RNA (gRNA) vectors using DNA cloning. These gRNA are intended to target the C-terminus of the SIN3 187-specific exon of the Sin3A gene. First, I annealed the top and bottom gRNA strands, which were ligated into the PU6-BbsI-chiRNA vector and then carried out transformation of chemically competent DH5α cells. Colonies were isolated from selective media agar plates. A DNA mini-prep was done to isolate the plasmids with the gRNA vectors and the successful ligation was confirmed with DNA sequence analysis. Next, these vectors will be used with the repair template donor vector to develop the LEXY system for SIN3 187 isoform. Generation of this new tool will allow us to investigate the phenotypic consequences of removal of a critical SIN3 isoform while allowing other isoforms to retain function.