|
| Status |
Public on Sep 02, 2014 |
| Title |
Histone H3 lysine-to-methionine mutants as a paradigm to study chromatin signaling |
| Organism |
Drosophila melanogaster |
| Experiment type |
Expression profiling by high throughput sequencing
|
| Summary |
Histone H3 lysine27-to-methionine (H3K27M) gain-of-function mutations occur in highly aggressive pediatric gliomas. Here, we establish a Drosophila animal model for the pathogenic histone H3K27M mutation and show that its overexpression resembles Polycomb repressive complex 2 (PRC2) loss-of-function phenotypes, causing de-repression of PRC2 target genes and developmental perturbations. Similarly, a H3K9M mutant depletes H3K9 methylation levels and suppresses position-effect variegation in various Drosophila tissues. The histone H3K9 demethylase KDM3B/JHDM2 associates with H3K9M nucleosomes and its overexpression in Drosophila results in loss of H3K9 methylation levels and heterochromatic silencing defects. Here we establish histone lysine-to-methionine mutants as robust in vivo tools for inhibiting methylation pathways that also function as biochemical reagents for capturing site-specific histone-modifying enzymes, thus providing molecular insight into chromatin-signaling pathways.
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| |
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| Overall design |
RNA-seq of wing imaginal discs expressing either H3.3WT-FLAG-HA or H3.3K27M-FLAG-HA.
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| Contributor(s) |
Herz HM, Morgan M, Gao X, Shilatifard A |
| Citation(s) |
25170156 |
| |
| Submission date |
Jul 29, 2014 |
| Last update date |
May 15, 2019 |
| Contact name |
Joan Conaway |
| E-mail(s) |
[email protected]
|
| Organization name |
Stowers Institute
|
| Street address |
1000 E 50th ST
|
| City |
Kansas City |
| State/province |
MO |
| ZIP/Postal code |
64110 |
| Country |
USA |
| |
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| Platforms (1) |
| GPL13304 |
Illumina HiSeq 2000 (Drosophila melanogaster) |
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| Samples (4)
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| Relations |
| BioProject |
PRJNA256995 |
| SRA |
SRP045072 |
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