Type of Submission
Poster
Keywords
Tetrahymena, mitotic regulation, H3K27, acetylation, gene regulation
Proposal
Diffuse intrinsic pontine glioma (DIPG) is a childhood cancer for which no effective treatments currently exist. DIPG patients have a point mutation in histone H3 resulting in lysine 27 being replaced by methionine. Since lysine residues on histone tails are sites for methylation and acetylation, common post-translational modifications which affect gene regulation, the lack of lysine at position 27 is correlated with dysregulated cell growth in DIPG. Since Tetrahymena thermophila have constitutively active growth pathways as well as homologs of histone H3 with lysine at position 27, we used these protozoans as a model system for studying the role of H3K27 in mitotic regulation. Using the antimitotic drug BAY-293, we found an increase in trimethylation at H3K27 as well as a statistically significant decrease in acetylation at H3K27 in cells that were exposed to BAY-293 when compared with DMSO controls. These data suggest that H3K27 is involved in gene silencing in Tetrahymena thermophila when exposed to BAY-293, indicating a role for H3K27 in mitotic regulation. Similar functions may be associated with H3K27 in other systems as well.
Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.
Publication Date
2023
H3K27 is Involved in Mitotic Regulation in Tetrahymena Thermophila
Diffuse intrinsic pontine glioma (DIPG) is a childhood cancer for which no effective treatments currently exist. DIPG patients have a point mutation in histone H3 resulting in lysine 27 being replaced by methionine. Since lysine residues on histone tails are sites for methylation and acetylation, common post-translational modifications which affect gene regulation, the lack of lysine at position 27 is correlated with dysregulated cell growth in DIPG. Since Tetrahymena thermophila have constitutively active growth pathways as well as homologs of histone H3 with lysine at position 27, we used these protozoans as a model system for studying the role of H3K27 in mitotic regulation. Using the antimitotic drug BAY-293, we found an increase in trimethylation at H3K27 as well as a statistically significant decrease in acetylation at H3K27 in cells that were exposed to BAY-293 when compared with DMSO controls. These data suggest that H3K27 is involved in gene silencing in Tetrahymena thermophila when exposed to BAY-293, indicating a role for H3K27 in mitotic regulation. Similar functions may be associated with H3K27 in other systems as well.
