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Repeat RNAs associate with replication forks and post-replicative DNA [long]

ABSTRACT: Non-coding RNA has a proven ability to direct and regulate chromatin modifications by acting as scaffolds between DNA and histone-modifying complexes. However, it is unknown if ncRNA plays any role in DNA replication and epigenome maintenance, including histone eviction and re-instalment of histone-modifications after genome duplication. Isolation of nascent chromatin has identified a large number of RNA-binding proteins in addition to unknown components of the replication and epigenetic maintenance machinery. Here, we isolated and characterized long and short RNAs associated with nascent chromatin at active replication forks and track RNA composition during chromatin maturation across the cell cycle. Shortly after fork passage, GA-rich-, Alpha repeats and TERRA RNA are associated with replicated DNA. These repeat RNAs arise from loci undergoing replication, suggesting an interaction in cis. Post-replication during chromatin maturation, and even after mitosis in G1, the repeats remain enriched on DNA. This argues that specific types of repeat RNAs are transcribed shortly after DNA replication and stably associates with their loci of origin throughout cell cycle. Our rich data set provides a resource to understand how repeat RNAs and their engagement with chromatin are regulated with respect to DNA replication and across the cell cycle.

ORGANISM(S): Homo sapiens

PROVIDER: GSE139219 | GEO | 2021/03/26

REPOSITORIES: GEO

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Repeat RNAs associate with replication forks and post-replicative DNA [short]

Project description:Non-coding RNA has a proven ability to direct and regulate chromatin modifications by acting as scaffolds between DNA and histone-modifying complexes. However, it is unknown if ncRNA plays any role in DNA replication and epigenome maintenance, including histone eviction and re-instalment of histone-modifications after genome duplication. Isolation of nascent chromatin has identified a large number of RNA-binding proteins in addition to unknown components of the replication and epigenetic maintenance machinery. Here, we isolated and characterized long and short RNAs associated with nascent chromatin at active replication forks and track RNA composition during chromatin maturation across the cell cycle. Shortly after fork passage, GA-rich-, Alpha repeats and TERRA RNA are associated with replicated DNA. These repeat RNAs arise from loci undergoing replication, suggesting an interaction in cis. Post-replication during chromatin maturation, and even after mitosis in G1, the repeats remain enriched on DNA. This argues that specific types of repeat RNAs are transcribed shortly after DNA replication and stably associates with their loci of origin throughout cell cycle. Our rich data set provides a resource to understand how repeat RNAs and their engagement with chromatin are regulated with respect to DNA replication and across the cell cycle.

2021-03-26 | GSE139351 | GEO

Two distinct modes for propagation of histone PTMs across the cell cycle

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Analysis of histone PTMs in nascent chromatin in new and old histones upon DNA damage (CAL353, CAL358) using the NCC-SILAC approach

Project description:Dynamic recycling and de novo deposition of histones are fundamental for chromatin restoration. Histone post-translational modifications (PTMs) are assumed to have a causal role in establishing distinct chromatin structures. However, it remains unknown how specific histone PTMs are regulated at broken replication fork. To get better insight into histone PTMs during DNA damage response, we combined NCC (Nascent chromatin capture) with SILAC-MS for identification of histone PTMs at replication forks upon CPT (camptothecin).

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DOT1L regulates pericentromeric heterochromatin

Project description:Many repetitive DNA elements are packaged in heterochromatin, but depend on occasional transcription to maintain long-term silencing. The factors that promote transcription of repeat elements in heterochromatin are largely unknown. Here, we show that DOT1L, a histone methyltransferase that modifies lysine 79 of histone H3 (H3K79), is required for transcription of major satellite repeats to maintain pericentromeric heterochromatin (PCH), and that this function is essential for preimplantation development. DOT1L is a transcriptional activator at single-copy genes but does not have a known role in repeat element transcription. We show that H3K79me3 is specifically enriched at repetitive elements, that loss of DOT1L compromises pericentromeric major satellite transcription, and that this function depends on interaction between DOT1L and the chromatin remodeler SMARCA5. DOT1L inhibition causes chromosome breaks and cell cycle defects, and leads to embryonic lethality. Together, our findings uncover a vital new role for DOT1L in transcriptional activation of heterochromatic repeats.

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Examination of three chromatin proteins in slivary glands in presence or absence of SuUR mutation using DamID technique

Project description:Heterochromatin contains repressively modified histones and replicates late in S phase of the cell cycle. Besides the shortage in replication origins, little is known about replication timing regulation in silenced regions. In Drosophila polytene cells, late replication results in under-replication and decreased DNA copy number in heterochromatic regions of the genome. The Suppressor of Under-replication (SUUR) protein controls this feature â?? in its absence the DNA polytenization level in most silenced regions is restored, however the repressive histone marks are lost. We hypothesized that SUUR regulates the re-establishment of repressive histone pattern during replication which results in delayed replication completion of heterochromatin. Measuring DNA copy number in mutants with disrupted repressive pathways, we found that under-replication is directly linked to repressive histone marks supply. DamID-seq and ChIP-seq experiments revealed that SuUR mutation does not affect the establishment of heterochromatin domains. Here, we identified a novel SUUR protein interaction (CG12018) that supports SUUR association with replication complex. SUUR loads onto replication forks shortly after the origin firing and participates in chromatin maintenance rather than its establishment. Thus, our findings provide comprehensive evidence that late replication in Drosophila is caused by the time-consuming process of replication-coupled repressive chromatin renewal. Examination of three chromatin proteins in slivary glands in presence or absence of SuUR mutation using DamID technique.

2016-01-10 | E-GEOD-74907 | biostudies-arrayexpress

Examination of H3K27me3 histone modification in 3 cell types in presence or absence of SuUR mutation

Project description:Heterochromatin contains repressively modified histones and replicates late in S phase of the cell cycle. Besides the shortage in replication origins, little is known about replication timing regulation in silenced regions. In Drosophila polytene cells, late replication results in under-replication and decreased DNA copy number in heterochromatic regions of the genome. The Suppressor of Under-replication (SUUR) protein controls this feature â in its absence the DNA polytenization level in most silenced regions is restored, however the repressive histone marks are lost. We hypothesized that SUUR regulates the re-establishment of repressive histone pattern during replication which results in delayed replication completion of heterochromatin. Measuring DNA copy number in mutants with disrupted repressive pathways, we found that under-replication is directly linked to repressive histone marks supply. DamID-seq and ChIP-seq experiments revealed that SuUR mutation does not affect the establishment of heterochromatin domains. Here, we identified a novel SUUR protein interaction (CG12018) that supports SUUR association with replication complex. SUUR loads onto replication forks shortly after the origin firing and participates in chromatin maintenance rather than its establishment. Thus, our findings provide comprehensive evidence that late replication in Drosophila is caused by the time-consuming process of replication-coupled repressive chromatin renewal. Examination of H3K27me3 histone modification in 3 cell types in presence or absence of SuUR mutation.

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Heterochromatin protein 1 (HP1) modulates replication timing of Drosophila heterochromatin

Project description:The replication of a genomic region during S-phase can be highly dynamic between cell types that differ in transcriptome and epigenome. Replication timing has been positively correlated with several histone modifications that occur at active genes, while repressive histone modifications mark late replicating regions. This raises the question if chromatin modulates the initiating events of replication. To gain insights into this question we have studied the function of heterochromatin protein 1 (HP1), a reader of to the repressive histone lysine 9 methylation of H3, in genome-wide organization of replication. Cells with reduced levels of HP1 show an advanced replication timing of centromeric repeats in agreement with the model that repressive chromatin mediates the very late replication of large clusters of constitutive heterochromatin. Surprisingly however regions with high levels of interspersed repeats on the chromosomal arms in particular on chromosome 4 and in pericentromeric regions of chromosome 2 behave differently. Here loss of HP1 results in delayed replication timing. The fact that these regions are bound by HP1 suggests a direct effect. Thus while HP1 mediates very late replication of centromeric DNA it is also required for early replication of autosomal regions with high levels of repeats. This observation of opposing functions of HP1 suggests a model where repeat inactivation on autosomes is required for proper activation of origins of replication that fire early, while HP1 mediated repression at constitutive heterochromatin is required to ensure replication of centromeric repeats at the end of S phase. Keywords: RNAi, chip-chip, replication timing

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Project description:Ubiquitination and epigenetic modification both play essential roles in regulating cell fates and development, but little is known how two pathways crosstalk. A known chromatin-binding protein BRWD3, Bromodomain repeats and WD40 repeats domain contain protein 3, has been shown involved both in ubiquitination and histone modification regulation. BRWD3 has roles in multiple chromatin-related processes, including transcription, DNA replication, and chromatin modification. However, how ubiquitination is involved and what’s BRWD3’s ubiquitination targets are barely known. Here, we study the single Drosophila homolog dBRWD3 to uncover its mechanism. To find dBRWD3’s ubiquitination targets, we performed both dBRWD3 IP-MS and BRWD3 dependent ubiquitination IP-MS. Expectedly, the whole BRWD3-Cul4-DDB1 E3 ubiquitination complex and multiple histones are significantly enriched in dBRWD3-IP. Interestingly, multiple histone modification writers and the DNA replication initiation factor origin recognition complex (ORC) are among the intersection of two MS. ORC’s function is highly dependent on chromatin signature. dBRWD3 could provide a perspective on how chromatin signature is regulated by ubiquitination to regulate ORC function. In support of this, about 35% of ORC2 binding sites overlap with dBRWD3 binding sites among the genome. The H3K27ac occupancy rate of dBRWD3 related ORC sites is about 50% higher than that of dBRWD3 irrelevant ORC sites. Depletion of dBRWD3 significantly reduces DNA proliferation in the S phase. Further study will focus on determining which histone modification writer is targeted for ubiquitination and how does it contribute to the chromatin signature and ORC function.

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Examination of SUUR and Pc chromatin proteins in slivary glands in presence or absence of SuUR mutation using DamID technique

Project description:Heterochromatin contains repressively modified histones and replicates late in S phase of the cell cycle. Besides the shortage in replication origins, little is known about replication timing regulation in silenced regions. In Drosophila polytene cells, late replication results in under-replication and decreased DNA copy number in heterochromatic regions of the genome. The Suppressor of Under-replication (SUUR) protein controls this feature – in its absence the DNA polytenization level in most silenced regions is restored, however the repressive histone marks are lost. We hypothesized that SUUR regulates the re-establishment of repressive histone pattern during replication which results in delayed replication completion of heterochromatin. Measuring DNA copy number in mutants with disrupted repressive pathways, we found that under-replication is directly linked to repressive histone marks supply. DamID-seq and ChIP-seq experiments revealed that SuUR mutation does not affect the establishment of heterochromatin domains. Here, we identified a novel SUUR protein interaction (CG12018) that supports SUUR association with replication complex. SUUR loads onto replication forks shortly after the origin firing and participates in chromatin maintenance rather than its establishment. Thus, our findings provide comprehensive evidence that late replication in Drosophila is caused by the time-consuming process of replication-coupled repressive chromatin renewal.

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