A5006621903- DNA Repair Mechanisms
- Microtubule and mitosis dynamics
- Epigenetics and DNA Methylation
- Genomics and Chromatin Dynamics
- Mitochondrial Function and Pathology
- Genetics, Aging, and Longevity in Model Organisms
- Cancer Genomics and Diagnostics
- Genetics and Neurodevelopmental Disorders
- CRISPR and Genetic Engineering
University of Geneva
2018-2025
Abstract DNA replication stress, a feature of human cancers, often leads to instability at specific genomic loci, such as the common fragile sites (CFSs). Cells experiencing stress may also exhibit mitotic synthesis (MiDAS). To understand physiological function MiDAS and its relationship CFSs, we mapped, high resolution, in cells treated with polymerase inhibitor aphidicolin. Sites were evident well-defined peaks that largely conserved between cell lines encompassed all known CFSs. The...
Abstract Histone H3.3, a major variant of canonical histone H3, is highly conserved and essential for viability or fertility in most lineages. In Caenorhabditis elegans, H3.3 expressed from five genes. Here, Delaney... Replication-independent histones replace nucleosomes act as important regulators chromatin function. H3 that remarkably across taxa distinguished by just four key amino acids. Most genomes contain two more genes expressing complete loss the protein usually causes sterility...
Cells experiencing DNA replication stress enter mitosis with under-replicated DNA, which activates a repair mechanism known as mitotic synthesis (MiDAS). Here we describe protocol to identify at genome wide and high resolution the genomic sites where MiDAS occurs in cells exposed aphidicolin. We use EdU incorporation label nascent cells, followed by isolation of EdU-labeled next-generation sequencing. For complete details on execution this protocol, please refer Groelly et al. (2022)1...