Guido Barzaghi

Abstract In eukaryotes, transcription factors (TFs) must continuously compete with nucleosomes to access their binding sites, leading to cell-to-cell variability in chromatin accessibility at regulatory regions. Although critical to understand enhancer function in transcription, the mechanisms that define how frequently an enhancer is active in a cell population remain unclear.

A study using single-cell 3D genome mapping reveals phenotypic convergence during mouse Kras-driven lung adenocarcinoma progression and prioritizes clinically actionable driver genes. This highlights the importance of cell-to-cell variation in chromatin architecture as a determinant of cancer evolution.

Abstract Single molecule footprinting profiles the heterogeneity of TF occupancy at cis-regulatory elements across cell populations at unprecedented resolution. The single molecule nature of the data in principle allows for observing the footprint of individual transcription factors and nucleosomes. However, we currently lack algorithms to quantify these occupancy patterns of chromatin binding factors in an automated way and without prior assumptions on their genomic location.