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Extrachromosomal DNA (microDNA) in Human, Mouse and Chicken

ABSTRACT: MicroDNAs are <400-base long extrachromosomal circles found in mammalian cells. Tens of thousands of microDNAs were found in all tissue types, including sperm. MicroDNAs arose preferentially from areas with high gene density, high GC content, high exon density, promoters with activating chromatin modifications and in sperm from the 5'UTR of full-length LINE-1 elements, but were depleted from lamin-associated heterochromatin. Furthermore, analysis of microDNAs from a set of human cancer cell lines revealed lineage-specific patterns of microDNA origins. A survey of microDNAs from chicken cell lines defective in various DNA repair proteins revealed that homologous recombination repair and non-homologous end joining repair pathways are not required for microDNA production. A deletion of the MSH3 protein, involved in DNA mismatch repair, resulted in a significant decrease in microDNA abundance specifically from non-CpG areas of the genome. Thus microDNAs arise as part of normal cellular physiology, either from DNA breaks associated with RNA metabolism or from replication slippage followed by mismatch repair.

ORGANISM(S): Mus musculus Homo sapiens Gallus gallus

PROVIDER: GSE68644 | GEO | 2015/05/08

SECONDARY ACCESSION(S): PRJNA283289

REPOSITORIES: GEO

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Extrachromosomal DNA (microDNA) in Human, Mouse and Chicken

Project description:MicroDNAs are <400-base long extrachromosomal circles found in mammalian cells. Tens of thousands of microDNAs were found in all tissue types, including sperm. MicroDNAs arose preferentially from areas with high gene density, high GC content, high exon density, promoters with activating chromatin modifications and in sperm from the 5'UTR of full-length LINE-1 elements, but were depleted from lamin-associated heterochromatin. Furthermore, analysis of microDNAs from a set of human cancer cell lines revealed lineage-specific patterns of microDNA origins. A survey of microDNAs from chicken cell lines defective in various DNA repair proteins revealed that homologous recombination repair and non-homologous end joining repair pathways are not required for microDNA production. A deletion of the MSH3 protein, involved in DNA mismatch repair, resulted in a significant decrease in microDNA abundance specifically from non-CpG areas of the genome. Thus microDNAs arise as part of normal cellular physiology, either from DNA breaks associated with RNA metabolism or from replication slippage followed by mismatch repair. Circular DNA profiling by high throughput sequencing. Five human, ten mouse and nine chicken samples are analyzed

2015-05-08 | E-GEOD-68644 | biostudies-arrayexpress

The Application of Topological Scores in the Identification of Protein Interactions

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HNPCC-Sys: Molecular Characterization of Lynch Syndromes

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Dual FAN1 activities stabilize the HTT CAG repeat

Project description:Recent data strongly suggest HTT CAG repeat expansion drives Huntington’s disease (HD) pathogenesis and that disease development is modulated by components of the DNA damage response (DDR) pathway. FAN1 has been identified as a major HD modifier which slows expansion of the HTT CAG repeat in several cell and animal HD models. Here we show dual FAN1 activities act to inhibit repeat expansion. A highly conserved SPYF motif in the FAN1 N-terminus is required for an MLH1 interaction, which slows expansion, with FAN1 nuclease activity also contributing towards repeat stabilisation. Our data supports a model where FAN1 binds MLH1, restricting its recruitment by MSH3 and the formation of the functional DNA mismatch repair (MMR) complex believed to promote CAG repeat expansion. FAN1 nuclease activity functions either concurrently or following MMR activity to maintain repeat stability. These data highlight a potential avenue for HD therapeutics in attenuating somatic expansion.

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High-resolution mapping of heteroduplex DNA formed in UV-induced and spontaneous mitotic recombination events in yeast

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MBD4 loss results in global reactivation of promoters and retroelements with low methylated CpG density.

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MBD4 loss results in global reactivation of promoters and retroelements with low methylated CpG density.

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Expression data from Saccharomyces cerevisiae strains carrying the rna14-1 or the rna15-1 allele

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