19th EDRA Webinar - March 17th, 2026

19th EDRA Webinar - March 17th, 2026, from 4:00 to 5:30 pm (CET)

Shana J. Sturla - Keynote speaker

Complex but not random? The chemistry and biology of mutagenesis

ETH Zürich, Zürich, Switzerland www.toxicology.ethz.ch

Alterations to the human genome arising from diverse forms of DNA modification, such as drug-induced alkylation and strand breakage to base oxidation, drive genome function, mutation patterns, and disease susceptibility. However, the complexity and context dependence of these lesions have made it difficult to understand how specific types of DNA damage and their genomic context impact biological consequences. We have advanced various strategies for high-resolution genomic mapping of discreet chemical alterations in the human genome in order to understand how the location, frequency, and persistence of different DNA lesions influence cellular outcomes. Using tailored chemical biology sequencing approaches, such as click-code-seq, we have uncovered distinct patterns of DNA damage across diverse genomic elements. These profiles are diagnostic of outcomes such as mutagenesis, the progression of biological aging and neurological function, thus offering new opportunities to explain how chemical modifications to the genome, molecular maintenance pathways and cellular outcomes connect as a basis of mechanisms of genome instability and disease.

Jérôme Poli - Short talk

Institute of Human Genetics, University of Montpellier, Montpellier, France

Transcription-Replication conflicts management by the S phase checkpoint

Replicative stress is one of the major causes of genomic instability promoting oncogenesis. Loss of coordination between the transcription and replication programs appears to be the major source of oncogene-induced replicative stress. Yet, how the transcription process hinders DNA replication remains poorly understood and several non-mutually exclusives hypotheses have to be considered : 1. Transcription machineries act as roadblocks; 2. Chromosomes association to the nuclear envelope forms topological barriers; 3. Transcription by-products such as RNA:DNA hybrids interfere with replication forks. Previously, our team identified the S phase checkpoint, as a key player shutting down RNA polymerase II (RNAPII) transcription during replication stress. Now, we combine genetics, high resolution microscopy and genome-wide approaches to pinpoint how the transcription process perturbs DNA replication. I will discuss the functional importance of transcription control by the S phase checkpoint during DNA replication.