The contributions of Polycomb Repressive Complex 2 and H3K27me3 on gene repression in Neurospora crassa
| dc.contributor.advisor | Selker, Eric | |
| dc.contributor.author | Kulawiec, Anna | |
| dc.contributor.author | Storck, Will | |
| dc.contributor.author | Selker, Eric | |
| dc.date.accessioned | 2020-08-11T17:29:57Z | |
| dc.date.available | 2020-08-11T17:29:57Z | |
| dc.date.issued | 2020 | |
| dc.description | Project files are comprised of 1 page pdf and presentation recording in mp4 format. | |
| dc.description.abstract | Though DNA contains our genes, the expression of genes varies during development and across different cellular conditions. Gene expression can be regulated by the post-translational protein modification of chromatin, such as the trimethylation of lysine 27 of histone 3 (H3K27me3). This mark, catalytically deposited by the protein complex Polycomb Repressive Complex 2 (PRC2), represses associated genes. Such repression is crucial for establishing gene expression patterns for proper development, and aberrant activity of PRC2 can cause disease, such as cancer. Here I present Neurospora crassa as a model organism for studying the repressive effects of PRC2, independent of its catalytic mark, H3K27me3. I generated a catalytically inactive SET-7, the catalytic component of PRC2 in N. crassa, demonstrating that elimination of H3K27me3 is sufficient to depress genes it normally marks despite the physical presence of PRC2. I further show that, in contrast to SET-7 knockout, catalytic inactivation of SET-7 does not alter the stability of PRC2. Moreover, catalytic inactivation of SET-7 enriches a higher molecular weight form of the core PRC2 member SUZ12. Overall, these results indicate that the physical form of PRC2 in itself does not act repressively and suggests that studies focusing on its repressive effects should consider that methods of H3K27me3 elimination, either knockout or catalytic inactivation, differentially affect PRC2 complex stability. This work provides valuable insights into the appropriate methodologies for studying developmental processes and disease related to PRC2 and H3K27me3. | en_US |
| dc.description.sponsorship | NIH, Undergraduate Research Opportunity Program, and the Clark Honors College Schwartzrock Family Thesis Research Grant | |
| dc.format.mimetype | video/mp4 | |
| dc.format.mimetype | application/pdf | |
| dc.identifier.orcid | https://orcid.org/0000-0003-3662-8812 | |
| dc.identifier.uri | https://hdl.handle.net/1794/25481 | |
| dc.language.iso | en_US | |
| dc.publisher | University of Oregon | |
| dc.rights | Creative Commons CC BY-NC-ND 4.0 | |
| dc.subject | molecular biology | en_US |
| dc.subject | epigenetics | en_US |
| dc.subject | biology | en_US |
| dc.title | The contributions of Polycomb Repressive Complex 2 and H3K27me3 on gene repression in Neurospora crassa | |
| dc.type | Presentation |