Sexual reproduction is a risky and complex process that can lead to DNA damage or cell death. Thus, organisms who sexually reproduce use intricate signal cascades to ensure reproduction proceeds smoothly. Yeast are an optimal system for studying reproduction because scientists have elucidated many of the mechanisms responsible for the correct progression of reproduction. In yeast, mating is one of the best understood forms of reproduction and meiosis. In budding yeast, two mating types (MT), a and a, exist; these opposite MTs mate, go through meiosis and form spores. However, when a cell is isolated without an opposite MT partner, it is unable to mate and form spores. To resolve this, yeast have evolved a mechanism, called mating-type switching (MTS), that allows an isolated cell to perform meiosis without a mating partner available. During MTS, yeast perform mitosis to form two identical cells. The mother cell then undergoes DNA rearrangement to switch to the opposite MT so the mother and daughter cell can mate. This rearrangement has significant risks and requires complex signal cascades to mitigate DNA damage. In some yeast species, the transcription factor STE12 is one of the molecules responsible for this regulation, and is upregulated during both mating and MTS. Our research focuses on MTS in the methylotrophic yeast Ogataea polymorpha, which is distantly related to the model yeast, Saccharomyces cerevisiae. While STE12 has been identified as both necessary and sufficient for inducing MTS in O. polymorpha, less is known about how STE12 controls the MTS signal cascade. Here, weinvestigated two pathways related to STE12-mediated MTS in O. polymorpha; the upstream pheromone response pathway and potential regulatory downstream long non- coding (lnc)RNAs. Previous research indicated that pheromones were not necessary to initiate the MTS signal cascade. However, it remains unclear whether pheromone exposure might suppress STE12-mediated MTS, because cells, sensing a mating partner was present, would divert their signal cascade towards mating rather than MTS. To test this hypothesis, we induced MTS in a cells and exposed the cultures to two variants of a pheromones. We saw qualitative suppression of MTS, leading us to develop a semi- quantitative PCR procedure to quantify suppression. Our semi-qPCR method correctly determined known cell mixture ratios, demonstrating the effectiveness of this method and making us confident in its use for future quantification. Based on the presence of regulatory lncRNAs in sexual processes in other yeast species, we hypothesized that lncRNAs may help regulate the MTS signal cascade in O. polymorpha. We performed an RNA-seq analysis on switched cells to identify putative lncRNAs regulated by STE12. We used a bioinformatics pipeline to identify novel transcripts upregulated by STE12. We found 5 upregulated lncRNAs, one of which was proximally located near an important MTS gene and potentially involved in its regulation. Because of their correlation with STE12 upregulation, these lncRNAs require further analysis to elucidate their potential roles in MTS. This study strengthens our general understanding of how sexual reproduction is transmitted, maintained and regulated.