My research is focused on understanding how epimutations in the paternal germline can potentiate cancer susceptibility in a transgenerational fashion. To investigate this hypothesis, I specifically induce such epimutations in mice by conditionally deleting Utx, a H3K27me3 demethylase, and characterise the molecular and phenotypic consequences in genetically wildtype offspring. Given that this epigenetic modifier is known to be active at bivalent domains in a developmental context, I am also investigating links between transgenerational phenotypes and potential changes to the poised state of sperm cells provoked by loss of Utx. Therefore, my research overlaps with two key themes of the Lesch lab: epigenetic memory and gene regulation via bivalent chromatin.