Detection of Somatic Mutations in vitro Aging Cells
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ABSTRACT:
PROVIDER: PRJNA554710 | ENA |
REPOSITORIES: ENA
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Project description:Detection of Somatic Mutations in vitro Aging Cells
| PRJNA554709 | ENA
Project description:<p>Deep sequencing was performed to analyze the prevalence of somatic mutations during <i>in vitro</i> cell aging. Primary dermal fibroblasts from healthy subjects of young and advanced age, from Hutchinson-Gilford progeria syndrome, and from Xeroderma Pigmentosum complementation group A (XPA) and C (XPC), were first restricted in number and then expanded <i>in vitro</i>. DNA was obtained from cells pre- and post-expansion and sequenced at high depth, over a cumulative 290 kb target region, including the exons of 44 aging-related genes. Allele frequencies of 58 somatic mutations differed between the pre- and post-cell culture expansion passages.</p>
| phs001867 | dbGaP
Project description:Studies on somatic mutations in cloned animals have revealed slight genetic variances between clones and their originals but have yet to identify the precise effects of these differences within the organism. Somatic mutations contribute to aging and are implicated in tumor development and other age-related diseases. To explore this, we compared whole genome sequencing data of an original dog with cloned dogs, identifying 8,155 candidate somatic mutations. By analyzing mutational signatures and rates within relevant genes, we identified potential associations with aging. Further analysis of 239 homozygous mutations within 189 genes revealed significant enrichment of traits related to chronotype, adult body size, height, spherical equivalent or myopia, and age at first sexual intercourse, suggesting these genes play roles in both growth and aging, as indicated by changes during adolescence.
2024-06-17 | E-MTAB-13924 | biostudies-arrayexpress
Project description:Somatic stem cells mediate tissue maintenance for the lifetime of an organism. Despite the well-established longevity that is a prerequisite for such function, accumulating data argue for compromised stem cell function with age. Identifying the mechanisms underlying age-dependent stem cell dysfunction is therefore key to understand the aging process. Using a model that carries a proofreading defective mitochondrial DNA polymerase, we demonstrate hematopoietic defects reminiscent of premature HSC aging including anemia, lymphopenia and myeloid lineage skewing. However, in contrast to physiologic stem cell aging, rapidly accumulating mitochondrial DNA mutations displayed little involvement of the hematopoietic stem cell pool but rather with distinct differentiation blocks and/or disappearance of downstream progenitors. Hematopoietic stem cells (HSC) has been sorted out from midaged wildtype and mutator mice and compared with stem cells sorted from young and and old wt mice
2011-05-06 | E-GEOD-27686 | biostudies-arrayexpress
Project description:Somatic mutations in individual skin cells
| PRJNA1125507 | ENA
Project description:Somatic mutations in individual skin cells
| PRJNA1125506 | ENA
Project description:Layer-specific somatic mutations in apricot
| PRJEB71142 | ENA
Project description:We report a novel approach to identify genome-wide somatic hypermutation hotspots from short Illumina H3K4me3 ChIPseq reads in diffuse large B-cell lymphoma cells (DLBCL). Abberant somatic hypermation are known to occur at the promoters of several proto-oncogenes in DLBCL. To identify such events genome-wide, we performed H3K4me3 ChIPseq experiments (as to enrich promoter sequences of actively transcribed genes) in 2 DLBCL cells lines (OCI-Ly1 and OCI-Ly8) and their normal B-cell counterparts, Naive B cells (NBC) and Germinal Center B cells (GCBs). We discover new genes that harbor mutations in their promoter regions that are potentially introduced by the aberrant activation-induced cytosine deaminase activity in lymphoma cell lines, and many of these genes are important for the B cell biology. Moreover, we show that these mutations can affect the activities of these promoters. Our study provides a feasible approach for the detection of promoter mutations and broadens our knowledge on promoter mutations in lymphomas. Examination of 1 histone mark (H3K4me3) in 4 different cell types.
2012-07-16 | E-GEOD-34316 | biostudies-arrayexpress
Project description:Somatic mutations in Parkinson disease are enriched in synaptic and neuronal processes
| PRJEB43918 | ENA
Project description:We report a novel approach to identify genome-wide somatic hypermutation hotspots from short Illumina H3K4me3 ChIPseq reads in diffuse large B-cell lymphoma cells (DLBCL). Abberant somatic hypermation are known to occur at the promoters of several proto-oncogenes in DLBCL. To identify such events genome-wide, we performed H3K4me3 ChIPseq experiments (as to enrich promoter sequences of actively transcribed genes) in 2 DLBCL cells lines (OCI-Ly1 and OCI-Ly8) and their normal B-cell counterparts, Naive B cells (NBC) and Germinal Center B cells (GCBs). We discover new genes that harbor mutations in their promoter regions that are potentially introduced by the aberrant activation-induced cytosine deaminase activity in lymphoma cell lines, and many of these genes are important for the B cell biology. Moreover, we show that these mutations can affect the activities of these promoters. Our study provides a feasible approach for the detection of promoter mutations and broadens our knowledge on promoter mutations in lymphomas.
2012-07-16 | GSE34316 | GEO