Dr Natalia Kunowska
Senior Research Assistant
This person is a member of Sanger Institute Alumni.
My main research interests are the molecular mechanisms underlying cell identity and function and their perturbation in disease. My scientific background is in studying gene and protein networks involved in transcriptional regulation and epigenetics. I am currently applying my knowledge of these fields to human genetics, to contribute to elucidating how non-coding variants can increase the risk of autoimmune diseases.
Currently, I am working on a project aiming to elucidate the molecular mechanism by which non-coding genetics variants associated with elevated risk of developing autoimmune diseases contribute to pathogenesis of these diseases. I am characterising the gene activity profiles and functioning of a rare subset of T lymphocytes, the regulatory T cells, obtained from healthy donors in order to be able to correlate different phenotypes with the underlying genotypes.
Previously, during my postdoctoral work at the MRC Clinical Sciences Centre at the Imperial College London, I focussed on studying gene regulation in B lymphocytes on a genome-wide scale. To understand how the histone code is “read” and translated into meaningful biological outcomes in the B cells, I characterised the proteins interacting with different combinations of modifications on histone proteins, which lead to identification of a novel protein complex that can bind to and “read” the double histone mark H3K9me3S10ph. Using ChIP-sequencing I studied how the identity of primary resting B lymphocytes is established through cooperation of transcription factors and chromatin modifiers. In my postdoc, I also collaborated on two studies investigating the role of Polycomb group of developmental proteins in stemness and differentiation.
I had my first experiences in the fields of gene regulation and epigenetics during my PhD work at Freiburg University, which focused on the chromatin-based mechanisms involved in regulating the gene activity during the development of cancer. I described a novel interactor of the major tumour suppressor protein p53, which represses histone acetylation at p53 target genes, thereby attenuating the p53-dependent anti-tumour response. I also participated in the discovery of new chromatin marks, H3T11ph and H3T6ph and in elucidating the cross-talk between histone phosphorylation and demethylation and its relevance in the prostate cancer.