Gene expression, which is essential for cell function, can be controlled by packing of DNA into domains of accessible or inaccessible DNA. In eukaryotic cells, DNA is wrapped around histone proteins to form chromatin. Heterochromatin, is one type of chromatin that is packaged tightly and inaccessible for transcription. It is heavily modified to reduce accessibility of DNA to make large regions of chromatin transcriptionally silent. Modification of the 9th lysine of histone H3, repressive histone methylation, propagates along heterochromatin causing transcriptional silencing; unlimited spread of this repressive H3K9me will improperly silence neighboring regions of chromatin, thus interfering with gene expression. In eukaryotes like Schizosaccharomyces pombe, the spread of silencing can be prevented by specific DNA elements called boundary elements. Some boundary elements require the action of the RNA polymerase III transcription factor, TFIIIC. However, other factors critical for TFIIIC-dependent boundary element function remain unknown. Previously, our research employed a genetic screen and identified ten mutants that are potential regulators of this pathway. We confirmed by Sanger sequencing that four screen hits contained mutations in the following genes: sda1, cog5, SPNCRNA.189, and vac7. Also, to test that these mutants had impaired boundary function, we quantified levels of H3K9me over a reporter gene that monitored boundary activity in these four mutagenized strains. Preliminary ChIP assays on the original mutagenized strains showed three mutants, sda1, cog5, and vac7, had more repressive histone methylation over the boundary reporter gene than in the wild type reporter strain where the boundary elements was still functional. Also, to confirm that the effects we had observed in the original mutagenesis were due to the identified point mutations, we attempted to use the CRISPR/Cas9 system and homologous recombination to reintroduce the identified mutants into boundary function reporter strains. Though each cloning technique used will need optimization, we successfully deleted SPNCRNA.189 by homologous recombination. In the future, ChIP analysis on the boundary reporter strain re-introduced with candidate mutants will help identify factors that contribute to boundary function and give insight to mechanisms by which boundary elements limit the spread of repressive histone methylation.