Epigenetic control and inheritance of rDNA arrays [3]
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PROVIDER: PRJNA1309134 | ENA |
REPOSITORIES: ENA
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Project description:Epigenetic control and inheritance of rDNA arrays [1]
| PRJNA1309023 | ENA
Project description:Epigenetic control and inheritance of rDNA arrays [2]
| PRJNA1309018 | ENA
Project description:Ribosomal RNA (rRNA) genes exist in multiple copies arranged in tandem arrays known as ribosomal DNA (rDNA). The total number of gene copies is variable, and the mechanisms buffering this copy number variation remain unresolved. We surveyed the number, distribution, and activity of rDNA arrays at the level of individual chromosomes across multiple human and primate genomes. Each individual possessed a unique fingerprint of copy number distribution and activity of rDNA arrays. In some cases, entire rDNA arrays were transcriptionally silent. Silent rDNA arrays showed reduced association with the nucleolus and decreased interchromosomal interactions, indicating that the nucleolar organizer function of rDNA depends on transcriptional activity. Methyl-sequencing of flow-sorted chromosomes, combined with long read sequencing, showed epigenetic modification of rDNA promoter and coding region by DNA methylation. Silent arrays were in a closed chromatin state, as indicated by the accessibility profiles derived from Fiber-seq. Removing DNA methylation restored the transcriptional activity of silent arrays. Array activity status remained stable through the iPS cell re-programming. Family trio analysis demonstrated that the inactive rDNA haplotype can be traced to one of the parental genomes, suggesting that the epigenetic state of rDNA arrays may be heritable. We propose that the dosage of rRNA genes is epigenetically regulated by DNA methylation, and these methylation patterns specify nucleolar organizer function and can propagate transgenerationally.
2025-08-25 | GSE306059 | GEO
Project description:Ribosomal RNA (rRNA) genes exist in multiple copies arranged in tandem arrays known as ribosomal DNA (rDNA). The total number of gene copies is variable, and the mechanisms buffering this copy number variation remain unresolved. We surveyed the number, distribution, and activity of rDNA arrays at the level of individual chromosomes across multiple human and primate genomes. Each individual possessed a unique fingerprint of copy number distribution and activity of rDNA arrays. In some cases, entire rDNA arrays were transcriptionally silent. Silent rDNA arrays showed reduced association with the nucleolus and decreased interchromosomal interactions, indicating that the nucleolar organizer function of rDNA depends on transcriptional activity. Methyl-sequencing of flow-sorted chromosomes, combined with long read sequencing, showed epigenetic modification of rDNA promoter and coding region by DNA methylation. Silent arrays were in a closed chromatin state, as indicated by the accessibility profiles derived from Fiber-seq. Removing DNA methylation restored the transcriptional activity of silent arrays. Array activity status remained stable through the iPS cell re-programming. Family trio analysis demonstrated that the inactive rDNA haplotype can be traced to one of the parental genomes, suggesting that the epigenetic state of rDNA arrays may be heritable. We propose that the dosage of rRNA genes is epigenetically regulated by DNA methylation, and these methylation patterns specify nucleolar organizer function and can propagate transgenerationally.
2025-08-25 | GSE306056 | GEO
Project description:Ribosomal RNA (rRNA) genes exist in multiple copies arranged in tandem arrays known as ribosomal DNA (rDNA). The total number of gene copies is variable, and the mechanisms buffering this copy number variation remain unresolved. We surveyed the number, distribution, and activity of rDNA arrays at the level of individual chromosomes across multiple human and primate genomes. Each individual possessed a unique fingerprint of copy number distribution and activity of rDNA arrays. In some cases, entire rDNA arrays were transcriptionally silent. Silent rDNA arrays showed reduced association with the nucleolus and decreased interchromosomal interactions, indicating that the nucleolar organizer function of rDNA depends on transcriptional activity. Methyl-sequencing of flow-sorted chromosomes, combined with long read sequencing, showed epigenetic modification of rDNA promoter and coding region by DNA methylation. Silent arrays were in a closed chromatin state, as indicated by the accessibility profiles derived from Fiber-seq. Removing DNA methylation restored the transcriptional activity of silent arrays. Array activity status remained stable through the iPS cell re-programming. Family trio analysis demonstrated that the inactive rDNA haplotype can be traced to one of the parental genomes, suggesting that the epigenetic state of rDNA arrays may be heritable. We propose that the dosage of rRNA genes is epigenetically regulated by DNA methylation, and these methylation patterns specify nucleolar organizer function and can propagate transgenerationally.
2025-08-26 | GSE306108 | GEO
Project description:Ribosomal RNA (rRNA) genes exist in multiple copies arranged in tandem arrays known as ribosomal DNA (rDNA). The total number of gene copies is variable, and the mechanisms buffering this copy number variation remain unresolved. We surveyed the number, distribution, and activity of rDNA arrays at the level of individual chromosomes across multiple human and primate genomes. Each individual possessed a unique fingerprint of copy number distribution and activity of rDNA arrays. In some cases, entire rDNA arrays were transcriptionally silent. Silent rDNA arrays showed reduced association with the nucleolus and decreased interchromosomal interactions, indicating that the nucleolar organizer function of rDNA depends on transcriptional activity. Methyl-sequencing of flow-sorted chromosomes, combined with long read sequencing, showed epigenetic modification of rDNA promoter and coding region by DNA methylation. Silent arrays were in a closed chromatin state, as indicated by the accessibility profiles derived from Fiber-seq. Removing DNA methylation restored the transcriptional activity of silent arrays. Array activity status remained stable through the iPS cell re-programming. Family trio analysis demonstrated that the inactive rDNA haplotype can be traced to one of the parental genomes, suggesting that the epigenetic state of rDNA arrays may be heritable. We propose that the dosage of rRNA genes is epigenetically regulated by DNA methylation, and these methylation patterns specify nucleolar organizer function and can propagate transgenerationally.
| S-EPMC11451732 | biostudies-literature
Project description:The germline is unique because it is the only cellular lineage capable of transferring genetic information from one generation to the next. Intergenerational transmission of epigenetic memory is also possible; however, in mammals this is largely prevented by extensive epigenetic erasure during germline definition from somatic precursors. We report that the ‘preformed’ germline of zebrafish, defined by inheritance of cellular components from the egg and not cellular reprogramming, shows consistently high levels of DNA methylation throughout development. This demonstrates epigenetic erasure is not a barrier to transgenerational epigenetic inheritance in zebrafish and likely other vertebrates with preformed germlines. Our analysis also uncovered female-specific germline amplification and demethylation of an 11.5-kb repeat region encoding 45S ribosomal RNA (fem-rDNA). The peak of fem-rDNA expansion coincided with the initial expansion of stage IB oocytes, the poly-nucleolar cell type responsible for zebrafish feminisation. Given that fem-rDNA overlaps with the only zebrafish locus identified thus far as sex-linked, we hypothesize fem-rDNA expansion is intrinsic to sex determination in this species.
2018-11-20 | GSE122695 | GEO
Project description:The ability of environmental exposures in one generation to elicit phenotypic outcomes in subsequent generations suggests that DNA is not the sole vehicle of biological heredity. Such non-genetic inheritance has been demonstrated in a variety of non-mammalian species but, to date, has remained controversial and inadequately characterised in mammals. Here, we show that early life protein restriction (PR) in mice alters DNA methylation at specific genetic variants of multi-copy ribosomal DNA (rDNA), to produce a linear correlation with the extent of growth restriction induced by PR. These effects are common to soma and germ-line and are concomitant with changes in the relative abundance of the responsive rDNA genetic variant. Intergenerational pedigree analysis reveals that rDNA genetic correlations are abolished between directly exposed males and their unexposed offspring, and epigenetic correlations are gained. To the best of our knowledge, this is the first direct demonstration in mammals of epigenetic dynamics induced by gene-environment interactions. Our work confirms rDNA as an evolutionarily conserved target of nutritional insults and intergenerational effects in flies, yeast, and now mice.
2016-07-08 | GSE72609 | GEO
Project description:The ability of environmental exposures in one generation to elicit phenotypic outcomes in subsequent generations suggests that DNA is not the sole vehicle of biological heredity. Such non-genetic inheritance has been demonstrated in a variety of non-mammalian species but, to date, has remained controversial and inadequately characterised in mammals. Here, we show that early life protein restriction (PR) in mice alters DNA methylation at specific genetic variants of multi-copy ribosomal DNA (rDNA), to produce a linear correlation with the extent of growth restriction induced by PR. These effects are common to soma and germ-line and are concomitant with changes in the relative abundance of the responsive rDNA genetic variant. Intergenerational pedigree analysis reveals that rDNA genetic correlations are abolished between directly exposed males and their unexposed offspring, and epigenetic correlations are gained. To the best of our knowledge, this is the first direct demonstration in mammals of epigenetic dynamics induced by gene-environment interactions. Our work confirms rDNA as an evolutionarily conserved target of nutritional insults and intergenerational effects in flies, yeast, and now mice.
2016-07-08 | GSE72608 | GEO
Project description:The ability of environmental exposures in one generation to elicit phenotypic outcomes in subsequent generations suggests that DNA is not the sole vehicle of biological heredity. Such non-genetic inheritance has been demonstrated in a variety of non-mammalian species but, to date, has remained controversial and inadequately characterised in mammals. Here, we show that early life protein restriction (PR) in mice alters DNA methylation at specific genetic variants of multi-copy ribosomal DNA (rDNA), to produce a linear correlation with the extent of growth restriction induced by PR. These effects are common to soma and germ-line and are concomitant with changes in the relative abundance of the responsive rDNA genetic variant. Intergenerational pedigree analysis reveals that rDNA genetic correlations are abolished between directly exposed males and their unexposed offspring, and epigenetic correlations are gained. To the best of our knowledge, this is the first direct demonstration in mammals of epigenetic dynamics induced by gene-environment interactions. Our work confirms rDNA as an evolutionarily conserved target of nutritional insults and intergenerational effects in flies, yeast, and now mice.
2016-07-08 | GSE72607 | GEO