Arrested replication forks guide retrotransposon integration
Ontology highlight
ABSTRACT:
ORGANISM(S): Schizosaccharomyces pombe
PROVIDER: GSE67692 | GEO | 2015/09/25
SECONDARY ACCESSION(S): PRJNA280702
REPOSITORIES: GEO
Similar Datasets
Project description:Transposable elements have the potential to act as controlling elements to influence the expression of genes. The current paradigm suggests that heterochromatic silencing can spread beyond the borders of the transposable element and influence the chromatin state of neighboring low-copy sequences. This would allow transposable elements to condition obligatory or facilitated epialleles and act as controlling elements. The maize genome contains numerous families of class I transposable elements (retrotransposons) that are present in moderate to high copy numbers and many are found in regions near genes which provides an opportunity to test whether the spreading of heterochromatin from retrotransposons is prevalent. We have investigated the extent of heterochromatin spreading into flanking DNA around each family of retrotransposons through profiling of DNA methylation and di-methylation of lysine 9 of histone 3 (H3K9me2) in low-copy regions of the maize genome. The effects of different retrotransposon families on local chromatin are highly variable. Some LTR families exhibit enrichment of heterochromatic marks within 800-1200 base pairs of the insertion site while other families have very little evidence for spreading of heterochromatic marks. The analysis of chromatin state in genotypes that lack specific insertions suggests that the adjacent heterochromatin results from spreading of silencing rather than insertion-site preferences. Genes that are located near elements that exhibit spreading of heterochromatin tend to be expressed at lower levels than other genes. Our findings suggest that a subset of LTR retrotransposon families may act as controlling elements influencing neighboring sequences while the majority of elements have little effect on flanking sequences Transposable elements comprise a substantial portion of many eukaryotic genomes. These mobile fragments of DNA can result in mutations through insertions into genes but may also affect the regulation of genes they insert near. There is evidence that the majority of transposable elements are epigenetically silenced and in some cases this silencing may affect neighboring sequences. However, evolutionary theory would predict that there would be selective pressures for transposable elements to limit their effects on neighboring genes. The maize genome has a complex organization with many genes flanked by retrotransposons. We profiled the spread of heterochromatin from the retrotransposons into nearby low copy sequences for 150 high copy retrotransposon families. While the manymajority of retrotransposons exhibit little to no spreading of heterochromatin there are a small number ofsome retrotransposon families that influence the chromatin state of surrounding regions. The families may represent bad “neighbors” that spread heterochromatin and influence nearby genes. 6 total samples: 3 replicates of B73 H3k9 and 3 replicates of Mo17 H3k9 3 total samples: mop1 mutant, b73.zmet2 (zmet2.m1 mutant in B73 background) and mo17.zmet2 (zmet2.m1 mutant in Mo17 background)
2012-11-26 | E-GEOD-39460 | biostudies-arrayexpress
Project description:Transposable elements have the potential to act as controlling elements to influence the expression of genes. The current paradigm suggests that heterochromatic silencing can spread beyond the borders of the transposable element and influence the chromatin state of neighboring low-copy sequences. This would allow transposable elements to condition obligatory or facilitated epialleles and act as controlling elements. The maize genome contains numerous families of class I transposable elements (retrotransposons) that are present in moderate to high copy numbers and many are found in regions near genes which provides an opportunity to test whether the spreading of heterochromatin from retrotransposons is prevalent. We have investigated the extent of heterochromatin spreading into flanking DNA around each family of retrotransposons through profiling of DNA methylation and di-methylation of lysine 9 of histone 3 (H3K9me2) in low-copy regions of the maize genome. The effects of different retrotransposon families on local chromatin are highly variable. Some LTR families exhibit enrichment of heterochromatic marks within 800-1200 base pairs of the insertion site while other families have very little evidence for spreading of heterochromatic marks. The analysis of chromatin state in genotypes that lack specific insertions suggests that the adjacent heterochromatin results from spreading of silencing rather than insertion-site preferences. Genes that are located near elements that exhibit spreading of heterochromatin tend to be expressed at lower levels than other genes. Our findings suggest that a subset of LTR retrotransposon families may act as controlling elements influencing neighboring sequences while the majority of elements have little effect on flanking sequences Transposable elements comprise a substantial portion of many eukaryotic genomes. These mobile fragments of DNA can result in mutations through insertions into genes but may also affect the regulation of genes they insert near. There is evidence that the majority of transposable elements are epigenetically silenced and in some cases this silencing may affect neighboring sequences. However, evolutionary theory would predict that there would be selective pressures for transposable elements to limit their effects on neighboring genes. The maize genome has a complex organization with many genes flanked by retrotransposons. We profiled the spread of heterochromatin from the retrotransposons into nearby low copy sequences for 150 high copy retrotransposon families. While the manymajority of retrotransposons exhibit little to no spreading of heterochromatin there are a small number ofsome retrotransposon families that influence the chromatin state of surrounding regions. The families may represent bad “neighbors” that spread heterochromatin and influence nearby genes.
2012-11-26 | GSE39460 | GEO
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2013-01-01 | E-GEOD-41183 | biostudies-arrayexpress
Project description:We report polysomal RNA sequencing data (RNAseq), small RNAseq, and virus-like-particle (VLP) DNA sequencing (DNAseq) and ChIPseq data. Arabidopsis ddm1 mutants produce LTR retrotransposon transcripts that are processed into 21-22 nt easiRNAs by RNA-Dependent RNA polymerase 6 (RDR6). To test if 21-22 nt easiRNAs regulate transcription, translation and reverse transcription of LTR retrotransposons, we compared ddm1 and ddm1rdr6 in polysomal RNAseq, VLP DNAseq and ChIPseq data. We found a handful of ATHILA elements were differentially regulated in ddm1rdr6 for polysomal RNAseq, VLP DNAseq, and ChIPseq datasets. Using short read and long read technologies, we also profiled functional LTR retrotransposons that made full-length DNA by reverse transcription inside VLPs. Small RNAseq data were obtained in pollen and inflorescence tissues in wild-type and ddm1.
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Project description:The repressive capacity of cytosine DNA methylation is mediated by recruitment of silencing complexes by methyl-CpG binding domain (MBD) proteins. Unexpectedly, we discovered that a family of arthropod Copia retrotransposons have incorporated a host-derived MBD domain. We functionally demonstrate how retrotransposon encoded MBDs preferentially bind to CpG-dense methylated regions, which correspond to transposable element regions of the host genome, in the myriapod Strigamia maritima. Consistently, young MBD-encoding Copia retrotransposons (CopiaMBD) accumulate in regions with higher CpG-densities than other LTR-retrotransposons also present in the genome. This would suggest that retrotransposons use MBDs to integrate into heterochromatic regions in Strigamia, avoiding potentially harmful insertions into host genes. In contrast, CopiaMBD insertions in the spider Stegodyphus dumicola genome disproportionately accumulate in methylated gene bodies when compared to other spider LTR-retrotransposons. Given that transposons are not actively targeted by DNA methylation in the spider genome, this distribution bias would also support a role for MBDs in the integration process. Together, these data demonstrate that retrotransposons can co-opt host-derived epigenome readers, potentially harnessing the host epigenome landscape to advantageously tune the retrotransposition process.
2019-06-17 | GSE118012 | GEO
Project description:Retrotransposons are classified into long terminal repeat (LTR) or non-LTR retrotransoposons, and both types can mobilize in a “copy and paste” manner. Rice genome contains >40% of repetitive sequences or transposable elements (TEs) that scattered throughout the genome. TE activities are tightly regulated by distinct epigenetic mechanisms. Histone lysine methylation is catalyzed by SET domain group (SDG) protein and reversed by a family of Jumonji C (JmjC) domain-containing proteins. In rice, DNA methylation and histone methylation have been implicated in controlling copia-like LTR retrotransposon Tos17 activities. Whether any TEs are controlled by histone demethylase remains to be elusive. Here, we show that JMJ703 is a histone H3K4 specific demethylase in rice. Impaired JMJ703 disrupted genome-wide transcriptome and enhanced H3K4me3 resulting in pleiotropic defects. Two LINE elements, Karma and its N-terminal truncation were identified as direct targets of JMJ703 with increased frequency of transposition in jmj703, while Tos17 is unaffected. Our findings show that plants use H3K4me3 demethylase to constitutively remove active chromatin mark and maintain silencing status at a subset retrotransposons which localize in heterochromatin regions. Therefore, our work uncovers a novel mechanism to control retrotransposon activity by histone demethylation, which further strengthens the link between epigenetic silencing and genome stability.
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Project description:Schizosaccharomyces pombe Raw sequence reads of Tf1 insertions within Sap1+ and Sap1-1 mutant cells
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Project description:Transposon reactivation is an inherent danger in cells that lose epigenetic silencing during developmental reprogramming. In the mouse, LTR-retrotransposons, or endogenous retroviruses (ERV), account for most novel insertions and are expressed in the absence of histone H3 Lysine 9 trimethylation in preimplantation stem cells. We found abundant, 18 nt tRNA-derived small RNA (tRF) in these cells, and ubiquitously expressed 22 nt tRFs, that include the 3' terminal CCA of mature tRNAs, and target the tRNA primer binding site (PBS) essential for ERV reverse transcription. We show that the two most active ERV families, IAP and MusD/ETn, are major targets and are strongly inhibited by tRFs in retrotransposition assays. 22 nt tRFs post-transcriptionally silence coding-competent ERVs, while 18 nt tRFs specifically interfere with reverse transcription and retrotransposon mobility. The PBS offers a unique target to specifically inhibit LTR-retrotransposons and tRF-targeting is a potentially highly conserved mechanism of small RNA-mediated transposon control.
2017-06-29 | GSE82199 | GEO
Project description:Retrotransposable elements are genomic parasites that are both key drivers of evolution and the ancestors of retroviruses. Although host cells have developed numerous mechanisms to keep these elements in check, there is also evidence from yeast to mammals that stressed cells sometimes activate transposition. Here we show that the fission yeast tf2 retrotransposons are regulated by alternative transcription start site (TSS) usage. Which TSS is used is determined by nucleosome positioning, which is in turn controlled by the Fun30 chromatin remodelers Fft2 and Fft3. By maintaining a high level of nucleosome occupancy at retrotransposon-flanking Long Terminal Repeat (LTR) elements, Fft2 and Fft3 promote the use of a downstream TSS and the production of RNA incapable of reverse transcription and retrotransposition. More generally, we show that Fft2 and Fft3 are involved in repressing the transcriptional response to stress, of which retrotransposon activation is a part. Finally, we show that in stressed cells retrotransposon TSS usage switches, allowing the production of full-length retrotransposon RNA. We propose that allowing retrotransposon transcription from a nonproductive TSS allows for the rapid activation of these elements in times of stress, while preventing their uncontrolled proliferation in the genome.
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