1-20 of 325265
Follow your search
Access your saved searches in your account

Would you like to receive an alert when new items match your search?
Close Modal
Sort by
Journal
Journal
Journal Articles
Journal Articles
Journal Articles
Journal Articles
Journal Articles
Journal Articles
Journal Articles
Journal Articles
Journal Articles
Journal Articles
Journal Articles
Journal Articles
Journal Articles
Journal Articles
Journal Articles
Images
Organization of the genome into TADs is orchestrated by architectural prote...
Published: 15 December 2022
FIGURE 1. Organization of the genome into TADs is orchestrated by architectural proteins. ( A ) Diagram representation of a TAD that harbors subTADs in a nested configuration. Color gradient in each subTAD denotes chromatin interaction frequency as measured with Hi-C, and scarcity of chromatin con... More
Images
Tcf1 and Lef1 TFs shape genome organization on multiple scales. Hi-C heat m...
Published: 15 December 2022
FIGURE 2. Tcf1 and Lef1 TFs shape genome organization on multiple scales. Hi-C heat maps showing the impact of Tcf1/Lef1 deficiency on genome organization surrounding the Myb gene locus on the TAD ( A ), subTAD ( B ), and hub ( C ) scales. (A) illustrates a 1.2-Mbp TAD in WT and Tcf1/Lef1 double-knockout (dKO) naive CD8+ T cells, where rectangles with dotted blue lines denote Tcf1/Lef1-dependent interactions between subTADs. The Myb-containing subTAD (denoted with triangles with blue lines) is enlarged in (B), where triangles with cyan lines denote a chromatin interaction hub showing strong dependence on Tcf1 and Lef1. The hub is enlarged in (C), where rectangles with dotted lines highlight four Tcf1/Lef1-dependent chromatin interaction patches. Hi-C data are from Shan et al. ( 38 , 58 ) and displayed in 10-kb resolution, with arrows marking transcription orientation of key genes. ( D ) Molecular characteristics at the genomic element level, aligned with chromatin interaction anchors in (C). Shown are sequencing tracks of Tcf1 and CTCF binding, ChrAcc (determined with DNase sequencing), and H3K27ac marking active promoters/enhancers. Yellow bar highlights a cluster of Tcf1+CTCF+ cobound sites (also part of a super enhancer spanning Myb) showing Tcf1/Lef1-dependent CTCF recruitment, ChrAcc, and enhancer activity, and the intracluster chromatin interaction (patch #2 in C) shows Tcf1/Lef1 dependence. The ChrAcc/enhancer cluster shows Tcf1/Lef1-dependent interactions with Myb and Hbs1l promoter regions (patches #3 and #4 in C, respectively). Open bars with dotted blue lines denote a Tcf1+CTCF+ cobound site at the Myb promoter and a CTCF solo site in the Hbs1l intron, which form a strong, Tcf1/Lef1-dependent interaction loop (patch #1 in C), likely marking the boundaries of a semi-insulated hub. ( E ) Venn diagram showing Tcf1 peaks in naive CD8+ and TCM cells. Tcf1 ChIP-seq data in naive CD8+ and TCM cells are from Shan et al. (Refs. 38 , GSE164713, and 62 , GSE177064), respectively, and after mapping to the mm9 mouse genome, high-confidence Tcf1 binding sites were called with MACS2 by the requiring ≥4-fold enrichment over a negative control (i.e., Tcf1-deficient naive CD8+ T cells) and false discovery rate <0.05, with genomic regions on the blacklist removed. FIGURE 2. Tcf1 and Lef1 TFs shape genome organization on multiple scales. Hi-C heat maps showing the impact of Tcf1/Lef1 deficiency on genome organization surrounding the Myb gene locus on the TAD (A), subTAD (B), and hub (C) scales. (A) illustrates a 1.2-Mbp TAD in WT and Tcf1/Lef1 double-knockout (dKO) naive CD8+ T cells, where rectangles with dotted blue lines denote Tcf1/Lef1-dependent interactions between subTADs. The Myb-containing subTAD (denoted with triangles with blue lines) is enlarged in (B), where triangles with cyan lines denote a chromatin interaction hub showing strong dependence on Tcf1 and Lef1. The hub is enlarged in (C), where rectangles with dotted lines highlight four Tcf1/Lef1-dependent chromatin interaction patches. Hi-C data are from Shan et al. (38, 58) and displayed in 10-kb resolution, with arrows marking transcription orientation of key genes. (D) Molecular characteristics at the genomic element level, aligned with chromatin interaction anchors in (C). Shown are sequencing tracks of Tcf1 and CTCF binding, ChrAcc (determined with DNase sequencing), and H3K27ac marking active promoters/enhancers. Yellow bar highlights a cluster of Tcf1+CTCF+ cobound sites (also part of a super enhancer spanning Myb) showing Tcf1/Lef1-dependent CTCF recruitment, ChrAcc, and enhancer activity, and the intracluster chromatin interaction (patch #2 in C) shows Tcf1/Lef1 dependence. The ChrAcc/enhancer cluster shows Tcf1/Lef1-dependent interactions with Myb and Hbs1l promoter regions (patches #3 and #4 in C, respectively). Open bars with dotted blue lines denote a Tcf1+CTCF+ cobound site at the Myb promoter and a CTCF solo site in the Hbs1l intron, which form a strong, Tcf1/Lef1-dependent interaction loop (patch #1 in C), likely marking the boundaries of a semi-insulated hub. (E) Venn diagram showing Tcf1 peaks in naive CD8+ and TCM cells. Tcf1 ChIP-seq data in naive CD8+ and TCM cells are from Shan et al. (Refs. 38, GSE164713, and 62, GSE177064), respectively, and after mapping to the mm9 mouse genome, high-confidence Tcf1 binding sites were called with MACS2 by the requiring ≥4-fold enrichment over a negative control (i.e., Tcf1-deficient naive CD8+ T cells) and false discovery rate &lt;0.05, with genomic regions on the blacklist removed. More
Images
Projected working models of TFs acting cooperatively with architectural pro...
Published: 15 December 2022
FIGURE 3. Projected working models of TFs acting cooperatively with architectural proteins in T cell genome organization. T lineage-specific TFs bind to specific DNA sequences and create nucleosome-free elements. Taking Tcf1 as an example, Tcf1 may act alone based on its intrinsic architectural fu... More