About her Postdoctoral project

We explore cellular/molecular contexts at the root of resilience versus vulnerability of biological systems. An example we recently identified is how modulation of the stress support pathway switches resilience into vulnerability to WEE1 perturbation, and how this vulnerability is cell type specific (manuscript in prep). This contextualisation (conditioned by cell type and by quantitative stress support) is particularly interesting as WEE1 has distinct modes of action recently emerged, including regulation of an intact dNTP pool, histone levels, epigenetic processes, DNA repair, beside its established implication on cell cycle progression. We propose to use this example of cellular/molecular context to build a logical model combining mathematics with –omics and use this model to predict mechanisms governing the vulnerability versus resilience switch. Quantitative/qualitative approaches will be developed to contextualise the modelled network.