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Germline DNA replication timing shapes mammalian genome composition

ABSTRACT: Germline DNA replication timing shapes mammalian genome composition

PROVIDER: PRJNA432066 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6638980_1.fastq.gz	Fastqsanger.gz
	SRR6638980_2.fastq.gz	Fastqsanger.gz
	SRR6638990_1.fastq.gz	Fastqsanger.gz
	SRR6638990_2.fastq.gz	Fastqsanger.gz
	SRR6639000_1.fastq.gz	Fastqsanger.gz

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Germline DNA replication timing shapes mammalian genome composition

Project description:DNA Replication Timing (RT) has been suggested to play an important role in shaping the mammalian genome by affecting mutation rates. Previous analyses were limited in that they relied on somatic DNA RT profiles, while to fully understand the influences of RT on the mammalian genome, germ cell RT information is necessary, as only germline mutations are passed to offspring and thus affect genomic composition. Using an improved RT mapping technique that allows mapping the RT from limited amounts of cells, we measured RT from two stages in the mouse germline - primordial germ cells (PGCs) and spermatogonial stem cells (SSCs).

2018-06-26 | GSE109804 | GEO

Germline DNA replication timing shapes mammalian genome composition.

Project description:Mammalian DNA replication is a highly organized and regulated process. Large, Mb-sized regions are replicated at defined times along S-phase. Replication Timing (RT) is thought to play a role in shaping the mammalian genome by affecting mutation rates. Previous analyses relied on somatic RT profiles. However, only germline mutations are passed on to offspring and affect genomic composition. Therefore, germ cell RT information is necessary to evaluate the influences of RT on the mammalian genome. We adapted the RT mapping technique for limited amounts of cells, and measured RT from two stages in the mouse germline - primordial germ cells (PGCs) and spermatogonial stem cells (SSCs). RT in germline cells exhibited stronger correlations to both mutation rate and recombination hotspots density than those of RT in somatic tissues, emphasizing the importance of using correct tissues-of-origin for RT profiling. Germline RT maps exhibited stronger correlations to additional genetic features including GC-content, transposable elements (SINEs and LINEs), and gene density. GC content stratification and multiple regression analysis revealed independent contributions of RT to SINE, gene, mutation, and recombination hotspot densities. Together, our results establish a central role for RT in shaping multiple levels of mammalian genome composition.

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Project description:Mammalian Rif1 defines the architecture of replication-timing domains interactions through the three-dimensional organization of the nuclear volume. Deletion of RIf1 in mammalian cells causes an initial alteration of three-dimensional chromatin organization which impacts first on replication timing and genome stability, but has long-term indirect repercussions also on gene expression

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Project description:Single-cell replication profiling reveals stochastic regulation of the mammalian replication-timing program

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Single-cell replication profiling reveals stochastic regulation of the mammalian replication-timing program [population]

Project description:This study demonstrates the stochastic nature of DNA replication-timing regulation by measures genome-wide replication timing in single-cells

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Project description:This study demonstrates the stochastic nature of DNA replication-timing regulation by measures genome-wide replication timing in single-cells

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Project description:This study demonstrates the stochastic nature of DNA replication-timing regulation by measuring genome-wide replication timing in single-cells

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Project description:In multicellular organisms, developmental changes to replication timing occur in 400- 800 kb domains across half the genome. While clear examples of epigenetic control of replication timing have been described, a role for DNA sequence in mammalian replication timing has not been substantiated. To assess the role of DNA sequences in directing these changes, we profiled replication timing in mice carrying a genetically rearranged Human Chromosome 21 [Hsa21]. In two distinct mouse cell types, Hsa21 sequences maintained human-specific replication timing, except at points of Hsa21 rearrangement. Changes in replication timing at rearrangements extended up to 900 kb and consistently reconciled with the wild-type replication pattern at developmental boundaries of replication-timing domains. Our results demonstrate DNA sequencedriven regulation of Hsa21 replication timing during development and provide evidence that mammalian chromosomes consist of multiple independent units of replication timing regulation. Profile comparison of fibroblast and T-cell cultures from trans-chromosomic mice and human and mouse controls.

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Distinct classes of genes behave as either drivers or dependents of replication timing switches (Replication-Timing).

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mRNA aging shapes the Cap2 methylome in mammalian mRNA

Project description:mRNA aging shapes the Cap2 methylome in mammalian mRNA

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