Evidence of developmental escape from transcriptional-gene-silencing in MESSI retrotransposons
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PROVIDER: PRJEB31935 | ENA |
REPOSITORIES: ENA
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Project description:Evidence of developmental escape from transcriptional-gene-silencing in MESSI retrotransposons
| PRJEB32452 | ENA
Project description:The intent of the experiment was to infer, from tissue-specific PCR-free whole DNA sequencing analysis, the putative increase in DNA copy number of active LTR retrotransposons in shoot apical meristems of tomato (Solanum lycopersicum). For this, we performed two lanes of Illumina pair-end DNA-seq in meristems and leaves of M82 tomato line.
2019-06-14 | E-MTAB-7823 | biostudies-arrayexpress
Project description:The intent of the experiment was to infer, from transcriptome analysis, the occurrence of competent LTR retrotransposons in shoot apical meristems of Solanum lycopersicum. For this, we performed Illumina pair-end RNA-seq in M82 tomato samples of meristems, leaves and flowers. We also harvested meristems in plants subjected to long-term heat. In addition, we performed RNA-seq in meristems, leaves and flowers samples from Solanum pennellii, to aid phylogenetic interpretations.
2019-07-02 | E-MTAB-7939 | biostudies-arrayexpress
Project description:Asterix/Gtsf1 links tRNAs and piRNA silencing of retrotransposons
| PRJNA634754 | ENA
Project description:The mammalian inactive X-chromosome (Xi) is structurally distinct from all other chromosomes and serves as a model for higher order chromosome organization. The Xi lacks strong topologically associated domains and is instead organized into megadomains and superloops mediated in part by the noncoding loci, Dxz4 and Firre. Their functional significance is presently unclear, though one study suggests that they permit Xi genes to escape silencing. Here, we find that megadomains do not form before silencing spreads along the Xi. Deletional analysis shows that Dxz4, but not Firre, is required for megadomains. Surprisingly, however, deleting neither Dxz4 nor Firre impacts Xi silencing or gene escape. Nor does it affect Xi nuclear localization, stability, or H3K27 methylation. Furthermore, ectopic integration of Dxz4 and Xist is not sufficient to form megadomains on autosomes, thereby uncoupling megadomain formation from chromosomal silencing. We conclude that Dxz4 and megadomains are dispensable for Xi silencing and escape.
2018-10-31 | GSE116649 | GEO
Project description:RNAi is a conserved mechanism in which small interfering RNAs (siRNAs) guide the degradation of cognate RNAs, but also promote heterochromatin assembly at repetitive DNA elements such as centromeric repeats. However, the full extent of RNAi functions and its endogenous targets have not been explored. Here we show that in the fission yeast Schizosaccharomyces pombe, RNAi and heterochromatin factors cooperate to silence diverse loci, including sexual differentiation genes, genes encoding transmembrane proteins, and retrotransposons that are also targeted by the exosome RNA degradation machinery. In the absence of the exosome, transcripts are processed preferentially by the RNAi machinery, revealing widespread occurrence of siRNA clusters and corresponding increase in heterochromatin modifications across large domains. We show that the generation of siRNAs and heterochromatin assembly by RNAi is triggered by a mechanism involving the canonical poly(A) polymerase Pla1 and an associated RNA surveillance factor Red1, which also activate the exosome. Remarkably, siRNA production and heterochromatin modifications at genes are regulated by environmental growth conditions, and by developmental signals that induce gene expression during sexual differentiation. Our analyses uncover interplay between RNAi and the exosome that is conserved in higher eukaryotes, and show that differentiation signals modulate RNAi silencing to regulate developmental genes. 8 ChIP samples
2012-11-26 | E-GEOD-41642 | biostudies-arrayexpress
Project description:RNAi is a conserved mechanism in which small interfering RNAs (siRNAs) guide the degradation of cognate RNAs, but also promote heterochromatin assembly at repetitive DNA elements such as centromeric repeats. However, the full extent of RNAi functions and its endogenous targets have not been explored. Here we show that in the fission yeast Schizosaccharomyces pombe, RNAi and heterochromatin factors cooperate to silence diverse loci, including sexual differentiation genes, genes encoding transmembrane proteins, and retrotransposons that are also targeted by the exosome RNA degradation machinery. In the absence of the exosome, transcripts are processed preferentially by the RNAi machinery, revealing widespread occurrence of siRNA clusters and corresponding increase in heterochromatin modifications across large domains. We show that the generation of siRNAs and heterochromatin assembly by RNAi is triggered by a mechanism involving the canonical poly(A) polymerase Pla1 and an associated RNA surveillance factor Red1, which also activate the exosome. Remarkably, siRNA production and heterochromatin modifications at genes are regulated by environmental growth conditions, and by developmental signals that induce gene expression during sexual differentiation. Our analyses uncover interplay between RNAi and the exosome that is conserved in higher eukaryotes, and show that differentiation signals modulate RNAi silencing to regulate developmental genes. We sequenced 7 samples from Schizosaccharomyces pombe and 2 samples from Drosophila melanogaster.
2012-11-26 | E-GEOD-41634 | biostudies-arrayexpress
Project description:Transposable elements are entangled in a constant evolutionary arms race with their host genomes, constantly evolving ways to evade host silencing mechanisms. One silencing mechanism used by many distantly related eukaryotes is dependent on cytosine methylation, an epigenetic mark deposited by C5 cytosine methyltransferases (CMTs). Therefore, it is expected transposable elements would acquire mechanisms to escape from being targeted by cytosine methylation. Here we report how two distantly related eukaryotic lineages have incorporated CMTs into the coding regions of distinct retrotransposon classes. Three of these events have occurred in the dinoflagellates of the genus Symbiodinium, where these CMT-encoding retrotransposons show hundreds of insertions. In a case of convergent evolution, the charophyte Klebsormidium nitens shows an independent expansion of CMT encoding retrotransposons. Concomitantly, we find that Symbiodinium genomes show cytosine methylation patterns unlike any other eukaryote with most of the genome hypermethylated in CpGs, while targeted CH methylation accumulates on transposable elements. Similarly, K. nitens shows CHH and CHG targeted methylation on repressed transposable elements, while CpG methylation is concentrated in gene bodies and transposable elements. Furthermore, we demonstrate the ability of retrotransposon CMTs to de novo methylate CpGs, indicating a putative role in mimicking retrotranscribed DNA as host active genomic DNA. Our results show an unprecedented example of how retrotransposons incorporate host-derived genes involved in DNA methylation as a source of adaptation to their host epigenomic environments.
2018-04-11 | GSE104474 | GEO
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:X chromosome inactivation (XCI) silences most genes on one X chromosome in female mammals, but some genes escape XCI. To identify escape gene in vivo and to explore molecular mechanisms that regulate this process we analyzed the allele-specific expression and chromatin structure of X-linked genes in mouse tissues and cells with skewed XCI and distinguishable alleles based on single nucleotide polymorphisms. Using a new method to estimate allelic expression, we demonstrate a continuum between complete silencing and significant expression from the inactive X (Xi). Few genes (2-3%) escape XCI to a significant level and only a minority differs between mouse tissues, suggesting stringent silencing and escape controls. Allelic profiles of DNase I hypersensitivity and RNA polymerase II occupancy of genes on the Xi correlate with escape from XCI. Allelic binding profiles of the DNA binding protein CCCTC-binding factor (CTCF) in different cell types indicate that CTCF binding at the promoter correlates with escape. Importantly, CTCF binding at the boundary between escape and silenced domains may prevent the spreading of active escape chromatin into silenced domains. Examination of allelic expression in mouse hybrid tissues.
2015-02-20 | E-GEOD-59777 | biostudies-arrayexpress