Research activities

Exploration of the role of transcription in suppressing cellular toxicity and preserving genetic and epigenetic inheritance

Genome integrity is essential for accurate gene expression and epigenetic inheritance. Similarly, transcriptional arrest may challenge genomic stability, contributing to genetic and epigenetic defects and the mechanisms of ageing and disease. To better understand gene regulation processes as well as transcription irregularities that might be implicated in the etiology of rare human disorders such as Cockayne syndrome and Spinocerebellar Ataxias, advanced next generation sequencing approaches and their interplay are exploited. We use healthy human cells and compare them with cells derived from patients that exhibit persistent transcriptional arrest in response to different genotoxic agents. Our aim is to model genome-wide cellular responses to transcriptional arrest in the 3D chromatin background and delineate their mechanistic details in healthy vs deficient situations.

Functional characterization of transcriptional arrest-specific ‘interactomes’

The aim of this part of the research is to identify and characterize transcriptional arrest-specific “interactomes” of transcription factors and repair proteins whose function has been implicated in disease pathogenesis. The work involves studies on the specific interplay between damage-induced chromatin alterations and transcription/ repair complexes with the ultimate goal to decipher how transcription is affected by other DNA-related processes in response to genotoxic insults.

The central interest is on better understanding the mechanisms that safeguard gene expression and contribute to genome integrity. To this end, high-throughput quantitative proteomics approaches have been employed in combination with biochemical and cellular techniques to build protein-protein interaction maps of damage-induced transcriptional arrest specific ‘interactomes’ and study their ‘crosstalk’ in normal human cells and a large battery of patient derived cell lines.


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