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Status |
Public on Sep 12, 2017 |
Title |
ChIP Seq analysis of H3K4me3 and H3K79me3 in euploid and aneuploid Saccharomyces cerevisiae |
Organism |
Saccharomyces cerevisiae S288C |
Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
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Summary |
Aneuploidy and epigenetic alterations have long been associated with carcinogenesis, but it was unknown whether aneuploidy could disrupt the epigenetic states required for cellular differentiation. In this study, we found that ~3% of random aneuploid karyotypes in yeast disrupt the stable inheritance of silenced chromatin during cell proliferation. Karyotype analysis revealed that this phenotype was significantly correlated with gains of chromosomes III and X. Chromosome X disomy alone was sufficient to disrupt chromatin silencing and yeast mating-type identity as indicated by a lack of growth response to pheromone. The silencing defect was not limited to the cryptic mating type loci but was associated with global changes in histone modifications and chromatin localization of Sir2 histone deacetylase. The chromatin-silencing defect of disome X can be partially recapitulated by increasing the copy number of several genes on chromosome X. These results suggest that aneuploidy can directly cause epigenetic instability and disrupt cellular differentiation.
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Overall design |
WT haploid and disome X yeast strains were grown in YPD to mid-log phase and harvested for genome-wide ChIP studies of histone modifications H3K4me3 and H3K79me3 in duplicate.
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Contributor(s) |
Seidel C |
Citation missing |
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Submission date |
Apr 27, 2017 |
Last update date |
Jul 25, 2021 |
Contact name |
Wahid A Mulla |
E-mail(s) |
mwahid1@jhmi.edu
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Organization name |
Johns Hopkins University
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Street address |
855 North Wolfe Street
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City |
Baltimore |
State/province |
MD |
ZIP/Postal code |
21205 |
Country |
USA |
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Platforms (1) |
GPL23380 |
Illumina HiSeq 2500 (Saccharomyces cerevisiae S288C) |
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Samples (12)
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Relations |
BioProject |
PRJNA384583 |
SRA |
SRP105341 |