e-mail: belen.gomez@cabimer.es
Main Research lines
- Transcription-associated genetic instability and R-loops
- Mechanisms preventing irreversible replication fork arrest
- Functions of histone deacetylases in double-strand break (DSB) repair
e-mail: belen.gomez@cabimer.es
Main Research lines

Belén Gómez González’s research is focused on understanding the molecular mechanisms that safeguard genome stability, with particular emphasis on the interplay between DNA replication, transcription, and DNA damage repair pathways.
Her work has contributed to support that transcription is a major endogenous source of genome instability. She demonstrated that the widespread accumulation of co-transcriptional R-loops impairs replication fork progression on a genome-wide scale, making the S-phase checkpoint essential for cell viability. Through the development of advanced genetic tools for in vivo R-loop detection in yeast and human cells, she has made key contributions to the identification and functional characterization of multiple factors involved in R-loop prevention and resolution in eukaryotes, including the THO complex, Senataxin, DNA damage response components, post-replicative repair pathways, BRCA2, DDX5, and DICER.
During her postdoctoral training at Clare Hall Laboratories (UK), her research focused on the role of S-phase checkpoints in replication fork stabilization. By combining whole-genome sequencing approaches with classical genetics, she uncovered a novel role for histone deacetylases in the DNA damage sensitivity of checkpoint-deficient mutants. After returning to CABIMER, she continued investigating the molecular mechanisms underlying replication fork destabilization, collapse, and repair, recently uncovering that S-phase checkpoint protects from aberrant replication fork processing and degradation.
Since 2026, she has been an Associate Professor in the Department of Genetics at the University of Seville. Her current research at CABIMER focuses on the causes and consequences of DNA damage arising during DNA replication, including R-loops and other transcription-replication conflicts, as well as on the mechanisms of replication fork stabilization and DSB repair, with special emphasis on the role of histone deacetylases.
ORCID: 0000-0003-1655-8407
ResearcherID: B-2365-2014
Scopus: 16678982400
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