I have a lifelong interest in the genome function, with a focus on epigenetic mechanisms and DNA modifications. My encounter with DNA methylation started with the study of bacterial DNA methyltrasferases in the Saulius Klimasauskas laboratory (Vilnius, Lithuania), where we were working to reveal the principals of enzyme-DNA recognition. I later joined Adrian Bird's laboratory for doctoral studies focusing on the function of methyl-CpG binding protein 2 (MeCP2). Mutations in MECP2 gene cause Rett Syndrome, a severe neurological disorder. We discovered a new splice isoform for MeCP2 gene and showed that absence of MeCP2 gene results abnormalities in mitochondrial function in mouse model for Rett Syndrome. As a post-doctoral fellow in Nathaniel Heintz laboratory, I investigated DNA methylation in two neuronal cell types, Purkinje and granule cells, where a distinct chromatin organization has been observed by electron microscopy. Development of methodology for isolation of neuronal sub-populations allowed us to probe cell type specific differences in chromatin organization in highly homogenous fashion. The final result exceeded expectations by revealing the presence of a novel DNA modification. We further demonstrated that 5-hydroxymethylcytosine (5hmC) is enriched in neuronal cells and depleted in cancer cell lines, but we still do not know why. 5hmC is found distributed along the whole gene in actively transcribed genes and bound by MeCP2 in brain. My laboratory at the Ludwig Institute in Oxford explores a variety of questions focusing on identifying molecular mechanisms in the genome function, affected by DNA modifications. Education PhD , The University of Edinburgh, Wellcome Trust Centre of Cell Biology, 2004 BA, Biology, Vytautas Magnus University, Kaunas, Lithuania, 1999 I have a lifelong interest in the genome function, with a focus on epigenetic mechanisms and DNA modifications. My encounter with DNA methylation started with the study of bacterial DNA methyltrasferases in the Saulius Klimasauskas laboratory (Vilnius, Lithuania), where we were working to reveal the principals of enzyme-DNA recognition. I later joined Adrian Bird's laboratory for doctoral studies focusing on the function of methyl-CpG binding protein 2 (MeCP2). Mutations in MECP2 gene cause Rett Syndrome, a severe neurological disorder. We discovered a new splice isoform for MeCP2 gene and showed that absence of MeCP2 gene results abnormalities in mitochondrial function in mouse model for Rett Syndrome. As a post-doctoral fellow in Nathaniel Heintz laboratory, I investigated DNA methylation in two neuronal cell types, Purkinje and granule cells, where a distinct chromatin organization has been observed by electron microscopy. Development of methodology for isolation of neuronal sub-populations allowed us to probe cell type specific differences in chromatin organization in highly homogenous fashion. The final result exceeded expectations by revealing the presence of a novel DNA modification. We further demonstrated that 5-hydroxymethylcytosine (5hmC) is enriched in neuronal cells and depleted in cancer cell lines, but we still do not know why. 5hmC is found distributed along the whole gene in actively transcribed genes and bound by MeCP2 in brain. My laboratory at the Ludwig Institute in Oxford explores a variety of questions focusing on identifying molecular mechanisms in the genome function, affected by DNA modifications. Education PhD , The University of Edinburgh, Wellcome Trust Centre of Cell Biology, 2004 BA, Biology, Vytautas Magnus University, Kaunas, Lithuania, 1999

I have a lifelong interest in the genome function, with a focus on epigenetic mechanisms and DNA modifications. My encounter with DNA methylation started with the study of bacterial DNA methyltrasferases in the Saulius Klimasauskas laboratory (Vilnius, Lithuania), where we were working to reveal the principals of enzyme-DNA recognition. I later joined Adrian Bird's laboratory for doctoral studies focusing on the function of methyl-CpG binding protein 2 (MeCP2). Mutations in MECP2 gene cause Rett Syndrome, a severe neurological disorder. We discovered a new splice isoform for MeCP2 gene and showed that absence of MeCP2 gene results abnormalities in mitochondrial function in mouse model for Rett Syndrome. As a post-doctoral fellow in Nathaniel Heintz laboratory, I investigated DNA methylation in two neuronal cell types, Purkinje and granule cells, where a distinct chromatin organization has been observed by electron microscopy. Development of methodology for isolation of neuronal sub-populations allowed us to probe cell type specific differences in chromatin organization in highly homogenous fashion. The final result exceeded expectations by revealing the presence of a novel DNA modification. We further demonstrated that 5-hydroxymethylcytosine (5hmC) is enriched in neuronal cells and depleted in cancer cell lines, but we still do not know why. 5hmC is found distributed along the whole gene in actively transcribed genes and bound by MeCP2 in brain. My laboratory at the Ludwig Institute in Oxford explores a variety of questions focusing on identifying molecular mechanisms in the genome function, affected by DNA modifications. Education PhD , The University of Edinburgh, Wellcome Trust Centre of Cell Biology, 2004 BA, Biology, Vytautas Magnus University, Kaunas, Lithuania, 1999