Genome-Wide Approaches to Studying Yeast Chromatin Modifications

2011 ◽  
pp. 61-71 ◽  
Author(s):  
Dustin E. Schones ◽  
Kairong Cui ◽  
Suresh Cuddapah
Keyword(s):  
Chromatin Modifications ◽  
Approaches To Studying ◽  
Genome Wide

Genome-wide approaches to studying chromatin modifications

2008 ◽  
Vol 9 (3) ◽  
pp. 179-191 ◽  
Author(s):  
Dustin E. Schones ◽  
Keji Zhao
Keyword(s):  
Chromatin Modifications ◽  
Approaches To Studying ◽  
Genome Wide

scholarly journals Expanding the RNA alphabet: The expanding world of mRNA modifications

2016 ◽  
Vol 38 (2) ◽  
pp. 13-16
Author(s):  
Benjamin Delatte ◽  
François Fuks
Keyword(s):  
Gene Regulation ◽  
Oxidation Product ◽  
Eukaryotic Cells ◽  
Chromatin Modifications ◽  
Rna Modifications ◽  
Recent Advances ◽  
Genome Wide ◽  
Gene Transcripts

Our understanding of the post-transcriptional modifications that decorate mRNAs, a regulatory layer positioned between DNA and proteins, is in its infancy. Recent advances in genome-wide mapping of pseudouridine (), N6-methyladenosine (m6A), 5-methylcytosine (5mrC), its oxidation product 5-hydroxymethylcytosine (5hmrC), and N1-methyladenosine (m1A) have proven that these modifications unsuspectedly occur from dozens to thousands of different gene transcripts in eukaryotic cells. Therefore epigenetics cannot only be restricted to chromatin modifications, and, when studying gene regulation, one has to consider the expanding kingdom of RNA modifications, also known as the epitranscriptome.

scholarly journals Two roles for the yeast transcription coactivator SAGA and a set of genes redundantly regulated by TFIID and SAGA

2019 ◽  
Author(s):  
Rafal Donczew ◽  
Linda Warfield ◽  
Derek Pacheco ◽  
Ariel Erijman ◽  
Steven Hahn
Keyword(s):  
Dna Analysis ◽  
Promoter Sequence ◽  
Sequence Motif ◽  
Chromatin Modifications ◽  
Protein Coding ◽  
Multiple Components ◽  
Genome Wide ◽  
Highly Sensitive ◽  
Redundant Genes ◽  
Transcription Coactivator

AbstractDeletions within genes coding for subunits of the transcription coactivator SAGA caused strong genome-wide defects in transcription and SAGA-mediated chromatin modifications. In contrast, rapid SAGA depletion produced only modest transcription defects at 13% of protein-coding genes – genes that are generally more sensitive to rapid TFIID depletion. However, transcription of these “coactivator-redundant” genes is strongly affected by rapid depletion of both factors, showing the overlapping functions of TFIID and SAGA at this gene set. We suggest that this overlapping function is linked to TBP-DNA recruitment. The remaining 87% of expressed genes that we term “TFIID-dependent” are highly sensitive to rapid TFIID depletion and insensitive to rapid SAGA depletion. Genome-wide mapping of SAGA and TFIID found binding of both factors at many genes independent of gene class. DNA analysis suggests that the distinction between the gene classes is due to multiple components rather than any single regulatory factor or promoter sequence motif.

scholarly journals Morc3 silences endogenous retroviruses by enabling Daxx-mediated H3.3 incorporation

2020 ◽  
Author(s):  
Sophia Groh ◽  
Anna Viktoria Milton ◽  
Lisa Marinelli ◽  
Cara V. Sickinger ◽  
Heike Bollig ◽  
...  
Keyword(s):  
Binding Sites ◽  
Atp Hydrolysis ◽  
Chromatin Accessibility ◽  
Endogenous Retroviruses ◽  
Chromatin Modifications ◽  
Interaction Domain ◽  
Knock Out ◽  
Genome Wide ◽  
A Genome ◽  
Mammalian Genomes

ABSTRACTEndogenous retroviruses (ERVs) comprise a significant portion of mammalian genomes. Although, specific ERV loci feature regulatory roles for host gene expression, most ERV integrations are transcriptionally repressed by Setdb1 mediated H3K9me3 and DNA methylation. However, the protein network which regulates deposition of these chromatin modifications is still incompletely understood. Here, we performed a genome-wide sgRNA screen for genes involved in ERV silencing and identified the GHKL ATPase protein Morc3 as top scoring hit. Morc3 knock-out cells display de-repression, reduced H3K9me3 and increased chromatin accessibility of distinct ERV classes. We found that the GHKL ATPase domain of Morc3 is critical for ERV silencing, since mutants which cannot bind ATP, or which are defective in ATP hydrolysis cannot rescue the Morc3 ko phenotype. Proteomic analysis revealed that Morc3 mutant protein which cannot bind ATP fails to interact with the H3.3 chaperone Daxx. This interaction depends on Morc3 SUMOylation, as Daxx lacking the SUMO interaction domain shows reduced association with Morc3. Notably, in Morc3 ko cells, we observed strongly reduced H3.3 on Morc3 binding sites. Thus, our data demonstrate Morc3 as critical regulator of Daxx-mediated H3.3 incorporation to ERV regions.

scholarly journals The Drosophila Y chromosome affects heterochromatin integrity genome-wide

2017 ◽  
Author(s):  
Emily J. Brown ◽  
Alison H. Nguyen ◽  
Doris Bachtrog
Keyword(s):  
Y Chromosome ◽  
Sex Chromosome ◽  
Gene Activation ◽  
Chromatin Modifications ◽  
Active Chromatin ◽  
Genomic Distribution ◽  
Sexual Dimorphisms ◽  
Y Chromosomes ◽  
Genome Wide ◽  
Males And Females

AbstractThe Drosophila Y-chromosome is gene poor and mainly consists of silenced, repetitive DNA. Nonetheless, the Y influences expression of hundreds of genes genome-wide, possibly by sequestering key components of the heterochromatin machinery away from other positions in the genome. To test the influence of the Y chromosome on the genome-wide chromatin landscape, we assayed the genomic distribution of histone modifications associated with gene activation (H3K4me3), or heterochromatin (H3K9me2 and H3K9me3) in fruit flies with varying sex chromosome complements (X0, XY and XYY males; XX and XXY females). Consistent with the general deficiency of active chromatin modifications on the Y, we find that Y gene dose has little influence on the genomic distribution of H3K4me3. In contrast, both the presence and the number of Y-chromosomes strongly influence genome-wide enrichment patterns of repressive chromatin modifications. Highly repetitive regions such as the pericentromeres, the dot, and the Y chromosome (if present) are enriched for heterochromatic modifications in wildtype males and females, and even more strongly in X0 flies. In contrast, the additional Y chromosome in XYY males and XXY females diminishes the heterochromatic signal in these normally silenced, repeat-rich regions, which is accompanied by an increase in expression of Y-linked repeats. We find hundreds of genes that are expressed differentially between individuals with aberrant sex chromosome karyotypes, many of which also show sex-biased expression in wildtype Drosophila. Thus, Y-chromosomes influence heterochromatin integrity genome-wide, and differences in the chromatin landscape of males and females may also contribute to sex-biased gene expression and sexual dimorphisms.

scholarly journals Morc3 silences endogenous retroviruses by enabling Daxx-mediated histone H3.3 incorporation

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Sophia Groh ◽  
Anna Viktoria Milton ◽  
Lisa Katherina Marinelli ◽  
Cara V. Sickinger ◽  
Angela Russo ◽  
...  
Keyword(s):  
Chromatin Accessibility ◽  
Endogenous Retroviruses ◽  
Chromatin Modifications ◽  
Knock Out ◽  
Mutant Proteins ◽  
Guide Rna ◽  
Histone H3.3 ◽  
Genome Wide ◽  
A Genome ◽  
Mammalian Genomes

AbstractEndogenous retroviruses (ERVs) comprise a significant portion of mammalian genomes. Although specific ERV loci feature regulatory roles for host gene expression, most ERV integrations are transcriptionally repressed by Setdb1-mediated H3K9me3 and DNA methylation. However, the protein network which regulates the deposition of these chromatin modifications is still incompletely understood. Here, we perform a genome-wide single guide RNA (sgRNA) screen for genes involved in ERV silencing and identify the GHKL ATPase protein Morc3 as a top-scoring hit. Morc3 knock-out (ko) cells display de-repression, reduced H3K9me3, and increased chromatin accessibility of distinct ERV families. We find that the Morc3 ATPase cycle and Morc3 SUMOylation are important for ERV chromatin regulation. Proteomic analyses reveal that Morc3 mutant proteins fail to interact with the histone H3.3 chaperone Daxx. This interaction depends on Morc3 SUMOylation and Daxx SUMO binding. Notably, in Morc3 ko cells, we observe strongly reduced histone H3.3 on Morc3 binding sites. Thus, our data demonstrate Morc3 as a critical regulator of Daxx-mediated histone H3.3 incorporation to ERV regions.

scholarly journals The Drosophila Y Chromosome Affects Heterochromatin Integrity Genome-Wide

2020 ◽  
Vol 37 (10) ◽  
pp. 2808-2824 ◽  
Author(s):  
Emily J Brown ◽  
Alison H Nguyen ◽  
Doris Bachtrog
Keyword(s):  
Y Chromosome ◽  
Sex Chromosome ◽  
Gene Activation ◽  
Chromatin Modifications ◽  
Active Chromatin ◽  
Genomic Distribution ◽  
Sexual Dimorphisms ◽  
Y Chromosomes ◽  
Genome Wide ◽  
Males And Females

Abstract The Drosophila Y chromosome is gene poor and mainly consists of silenced, repetitive DNA. Nonetheless, the Y influences expression of hundreds of genes genome-wide, possibly by sequestering key components of the heterochromatin machinery away from other positions in the genome. To test the influence of the Y chromosome on the genome-wide chromatin landscape, we assayed the genomic distribution of histone modifications associated with gene activation (H3K4me3) or heterochromatin (H3K9me2 and H3K9me3) in fruit flies with varying sex chromosome complements (X0, XY, and XYY males; XX and XXY females). Consistent with the general deficiency of active chromatin modifications on the Y, we find that Y gene dose has little influence on the genomic distribution of H3K4me3. In contrast, both the presence and the number of Y chromosomes strongly influence genome-wide enrichment patterns of repressive chromatin modifications. Highly repetitive regions such as the pericentromeres, the dot, and the Y chromosome (if present) are enriched for heterochromatic modifications in wildtype males and females, and even more strongly in X0 flies. In contrast, the additional Y chromosome in XYY males and XXY females diminishes the heterochromatic signal in these normally silenced, repeat-rich regions, which is accompanied by an increase in expression of Y-linked repeats. We find hundreds of genes that are expressed differentially between individuals with aberrant sex chromosome karyotypes, many of which also show sex-biased expression in wildtype Drosophila. Thus, Y chromosomes influence heterochromatin integrity genome-wide, and differences in the chromatin landscape of males and females may also contribute to sex-biased gene expression and sexual dimorphisms.

scholarly journals DNA polymerase epsilon is required for heterochromatin maintenance in Arabidopsis

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Pierre Bourguet ◽  
Leticia López-González ◽  
Ángeles Gómez-Zambrano ◽  
Thierry Pélissier ◽  
Amy Hesketh ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Dna Polymerase ◽  
Chromatin Modifications ◽  
Dna Polymerase Epsilon ◽  
Replicative Stress ◽  
Genome Wide ◽  
Polymerase Epsilon ◽  
Heterochromatin Silencing ◽  
And Function ◽  
Heterochromatin Structure

Abstract Background Chromatin organizes DNA and regulates its transcriptional activity through epigenetic modifications. Heterochromatic regions of the genome are generally transcriptionally silent, while euchromatin is more prone to transcription. During DNA replication, both genetic information and chromatin modifications must be faithfully passed on to daughter strands. There is evidence that DNA polymerases play a role in transcriptional silencing, but the extent of their contribution and how it relates to heterochromatin maintenance is unclear. Results We isolate a strong hypomorphic Arabidopsis thaliana mutant of the POL2A catalytic subunit of DNA polymerase epsilon and show that POL2A is required to stabilize heterochromatin silencing genome-wide, likely by preventing replicative stress. We reveal that POL2A inhibits DNA methylation and histone H3 lysine 9 methylation. Hence, the release of heterochromatin silencing in POL2A-deficient mutants paradoxically occurs in a chromatin context of increased levels of these two repressive epigenetic marks. At the nuclear level, the POL2A defect is associated with fragmentation of heterochromatin. Conclusion These results indicate that POL2A is critical to heterochromatin structure and function, and that unhindered replisome progression is required for the faithful propagation of DNA methylation throughout the cell cycle.

Sign in / Sign up

Export Citation Format

Share Document