transcription start site
Definition
A transcription start site (TSS) is the precise genomic location where RNA polymerase begins synthesizing an RNA transcript from a DNA template. Typically located downstream of promoter elements, the TSS marks position +1 in gene annotation, with upstream sequences designated as negative and downstream as positive. Multiple TSSs can exist for a single gene, generating transcript isoforms with different 5' untranslated regions (5' UTRs). TSS identification is crucial for understanding gene regulation, as the region surrounding the TSS contains critical regulatory elements including TATA boxes, CAAT boxes, and transcription factor binding sites. TSS mapping techniques like CAGE-seq and TSS-seq enable genome-wide identification of active transcription initiation sites across different cell types and conditions.
Visualize transcription start site in Nodes Bio
Researchers can visualize transcription start sites within gene regulatory networks, connecting TSSs to upstream transcription factors, enhancers, and chromatin modifiers. Network graphs can reveal how multiple TSSs for the same gene respond differently to regulatory inputs, map TSS-specific regulatory circuits, and identify shared transcription factor binding patterns across co-regulated genes with similar TSS architectures.
Visualization Ideas:
- Gene regulatory networks showing transcription factors connected to their target gene TSSs with edge weights representing binding affinity
- Multi-layer networks comparing TSS usage patterns across different cell types or disease states
- Causal networks linking epigenetic modifications and chromatin accessibility at TSS regions to downstream gene expression changes
Example Use Case
A cancer researcher investigating tumor heterogeneity discovers that melanoma cells use alternative transcription start sites in the BRAF oncogene under different microenvironmental conditions. By mapping TSS usage patterns across single-cell RNA-seq data, they identify that hypoxic tumor regions preferentially utilize a downstream TSS that produces a more stable transcript isoform. Network analysis reveals this alternative TSS is regulated by HIF1α and associated transcription factors, suggesting a novel therapeutic vulnerability in the hypoxic tumor niche.