Table 1.
ChIP-seq alignment results using Bowtie 0.12.7 (Hg19).
Figure 1.
Chromosomal distribution and genomic location of Tat binding sites.
(A) Enrichment pattern of Tat-bound regions among individual chromosomes is shown as a bar chart. Percent of total Tat-binding sites (red bars) and what would be expected by random chance (blue bars) for each chromosome is shown. The asterisks denotes enrichment P-value<10−4. (B) Distribution of all Tat-binding peaks in relation to gene structure is shown as a pie chart. Intergenic regions are defined as at least 3 kb away from the start and end of any transcript.
Figure 2.
Tat binds mainly to DNA repeat elements.
(A) Distribution of Tat-binding peaks in repeat versus non-repeat elements is shown as a pie chart. (B) Distribution of Tat-binding peaks within repeat elements in Alu versus non-Alu sequences is shown as a pie chart. (C) Percent of Tat-binding peaks within individual repeat element subtypes is shown for the top 20 enriched elements.
Figure 3.
Analysis of Tat binding to Alu elements.
(A) Average P-value of Tat-binding profile centered at the start of Alu elements for all Tat-bound Alu elements is shown. The x axis depicts ±1 kb away from start of Tat-bound Alu elements in 100-bp intervals. The y axis denotes −log10 of Tat-binding enrichment P-value of ChIPed Tat DNA count over input DNA count. (B) Genome browser representation of Tat enrichment profile compared to the input DNA at a representative Alu element is shown. The peak height corresponds to read counts. (C) Distribution of Tat-bound Alu elements with respect to gene structure is shown as a pie chart.
Figure 4.
Functional annotation of Tat binding regions.
(A) The bar chart shows the distribution of the distances between Tat binding peaks and transcriptional start sites (TSS). Note that a Tat peak may be assigned to more than one gene. Functional annotation of (B) Tat-bound regions and (C) Tat-bound Alu elements, using gene ontology terms generated by Mouse Genome Informatics (MGI) from mouse homologous gene knock out phenotypes. The x-axis values are −log10 of binomial raw P-values.
Figure 5.
Gene expression profile of Jurkat-Tat cells.
(A) Gene ontology annotation of genes with more than two-fold change in expression using DAVID. (B) Relationships of gene expression and H3K9ac changes to Tat-binding are shown. Genes are arranged in descending order based on their expression in Jurkat-Tat versus Jurkat cells. Each row represents one gene. For H3K9ac ChIP-chip analysis, each column represents a 500-bp window, spanning −5.5 to +2.5 kb of annotated TSS. Moving average of H3K9ac enrichment in three consecutive 500-bp windows is shown in each column (right panel).
Figure 6.
Tat binding peaks in Jurkat-Tat cells are associated with specific cellular factors and chromatin marks in Jurkat cells.
(A) Percent of all Tat peaks in Jurkat-Tat cells that are bound by CBP, ETS1, RUNX1, H3K4me3 and/or H3K27me3 in Jurkat cells is shown. (B) Percent of Tat peaks at TSS in Jurkat-Tat cells that are bound by CBP, ETS1, RUNX1, H3K4me3 and H3K27me3 in Jurkat cells is shown. (C) Shown is the Tat enrichment profile at the ZNF143 gene promoter in Jurkat-Tat cells compared to CBP, ETS1, RUNX1, H3K4me3, H3K27me3 enrichment at the same genomic location in Jurkat cells. The peak heights (y-axis) correspond to read counts. The x-axis represents the genomic coordinates.