43 research outputs found
Additional file 1: of Single-cell genome-wide bisulfite sequencing uncovers extensive heterogeneity in the mouse liver methylome
Supplementary materials. The supplementary materials include Figures S1–S3, Tables S1–S3, and Supplementary Experimental Procedures. (PDF 473 kb
L'Écho : grand quotidien d'information du Centre Ouest
30 janvier 19321932/01/30 (A61).Appartient à l’ensemble documentaire : PoitouCh
Additional file 8: Figure S2. of Comprehensive transcriptional landscape of aging mouse liver
Representative subset (Meg3, Rian and Mirg) of maternally expressed and imprinted ncRNA locus, Dlk-Dio3, on chromosome 12 in UCSC Genome Browser overlaid with aligned reads from RNA-seq dataset. Blue = sense paired-end, red = antisense paired-end; Scale = 100 kb. (PDF 64 kb
Additional file 4: Table S4. of Comprehensive transcriptional landscape of aging mouse liver
List of top GO terms from upregulated differentially expressed genes used to make Fig.Ă‚Â 3a. (XLSX 198 kb
Age-related DNA methylation patterns at imprinted gene promoters in cerebral cortex.
<p>DNA methylation status in cerebral specific CpG sites within promoters of imprinted genes in young i.e., 6 months (a) and old i.e., 27 months (b) C57BL/6 mice. Each tickmark represents specific CpG sites within the imprinted promoter and each column represents the methylation status for each animal.</p
Myc-Dependent Genome Instability and Lifespan in <i>Drosophila</i>
<div><p>The Myc family of transcription factors are key regulators of cell growth and proliferation that are dysregulated in a large number of human cancers. When overexpressed, Myc family proteins also cause genomic instability, a hallmark of both transformed and aging cells. Using an <i>in vivo lacZ</i> mutation reporter, we show that overexpression of Myc in <i>Drosophila</i> increases the frequency of large genome rearrangements associated with erroneous repair of DNA double-strand breaks (DSBs). In addition, we find that overexpression of Myc shortens adult lifespan and, conversely, that Myc haploinsufficiency reduces mutation load and extends lifespan. Our data provide the first evidence that Myc may act as a pro-aging factor, possibly through its ability to greatly increase genome instability.</p></div
Age-related DNA methylation patterns at imprinted and non-imprinted gene promoters in liver.
<p>DNA methylation status in liver at specific CpG sites within promoters of imprinted genes of young, i.e. 6 months (a) and old, i.e. 27 months (b) C57BL/6 mice liver. Each tickmark represents specific CpG sites within the imprinted promoter and each column represents the methylation status for each animal.</p
Age-related DNA methylation patterns at non-imprinted gene promoters in cerebral cortex.
<p>DNA methylation status in cerebral cortex at specific CpG sites within promoters of non-imprinted genes of young, i.e. 6 months (a), and old, i.e. 27 months (b), C57BL/6 mice. Each tickmark represents specific CpG sites within the non-imprinted promoter and each column represents the methylation status for each animal.</p
DNA methylation patterns at imprinted and non-imprinted gene promoters in <i>Ercc-/d7</i> mutant mice.
<p>DNA methylation status in liver at specific CpG sites within promoters of imprinted genes of <i>WT</i> (a) and <i>Ercc-/d7</i> (b) mice liver (both 14 weeks of age). Each tickmark represents specific CpG sites within the imprinted promoter and each column represents the methylation status for each animal.</p
Myc overexpression increases mutation frequency.
<p>(A) Schematic representation of the <i>lacZ</i> reporter we used to quantitate mutation frequency, and potential mutation events that can occur in this transgene. Adapted from Garcia et al. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0074641#pone.0074641-Garcia3" target="_blank">[29]</a> (B) Western analyses showing 9-fold overexpression of Myc compared to the loading control of γ-tubulin. Samples are wing imaginal discs of the genotypes hs-FLP; <i>lacZ</i> #2/+; act>CD2>Gal4, UAS-GFP/+ (shown as “+”) and hs-FLP; <i>lacZ</i> #2/+; act>CD2>Gal4, UAS-GFP/UAS-Myc larvae (shown as “Myc”). Larvae were heat shocked (37°C) for 45 min during the 3<sup>rd</sup> larval instar and allowed to develop for 12 hours. Eight discs were loaded per lane. (C) <i>lacZ</i> mutation frequency of hs-FLP; <i>lacZ</i> #2/+; act>CD2>Gal4, UAS-GFP/+ (shown as “+”) and hs-FLP; <i>lacZ</i> #2/+; act>CD2>Gal4, UAS-GFP/UAS-Myc larvae (shown as “Myc”). Larvae are collected 3 days after a 45 minute heat shock at 37°C during the 1<sup>st</sup> instar larval stage and separated by sex. Experiments shown are from at least four biological repeats (D) <i>lacZ</i> mutation frequency of hs-FLP; <i>lacZ</i> #9/+; act>CD2>Gal4, UAS-GFP/+ (shown as “+”) and hs-FLP; <i>lacZ</i> #9/+; act>CD2>Gal4, UAS-GFP/UAS-Myc (shown as “Myc”) larvae. (E) A selection (at least 48) plasmids were chosen to digest with AvaI to determine plasmid size per experiment for hs-FLP; <i>lacZ</i> #2/+; act>CD2>Gal4, UAS-GFP/+ (shown as “+”) and hs-FLP; <i>lacZ</i> #2/+; act>CD2>Gal4, UAS-GFP/UAS-Myc (shown as “Myc”) larvae. Male and female data are shown separately for these analyses and do not show any differences in mutation spectra. White filled area of bar represents frequency of size change mutation (genome rearrangement), where as black solid area shows frequency of mutant plasmids that do not show a size change (point mutations). *indicates statistical significance of p<0.001 (student’s t-test).</p