GokceLab - Systems Neuroscience – Cell Diversity
Changes in the genome, called mutations, are the driving force of evolution. These mutations continue to shape us from the moment we begin life as a single cell to the end of our life by altering the genome of each cell. During development, these somatic mutations provide important benefits including fighting infections by developing B-cells antibody diversity, but they are also the underlying cause of almost all age-related diseases, particularly cancer and neurodegeneration. Yet, we do not know how many mutations accumulate in each cell and what the key mutagenic mechanisms are.
Our group aims to characterize genomic changes at single cell resolution and to reveal mutagenic mechanisms leading to diseases. We primarily use single-cell sequencing technologies to characterize phenotypes and use molecular biology and animal models to understand the effects of somatic mutations on disease pathologies.
Our major research focus is genomic instability in brain during post stroke pathologies and neurodegeneration. We use single-cell sequencing to measure the accumulation of genomic mutations in animal models. Our aim is to identify mechanisms leading to genomic instability in cell types of the brain and to develop therapies to slow genomic aging.
We use a combination of single cell transcriptomics, live imaging and molecular approaches to elucidate the cellular and molecular mechanisms regulating the interconnected vascular-glial-neuron triad.
Together with Jürgen Bernhagen, we also analyze B-cell development at the single-cell resolution, as they are a key player in cardiovascular disease and atherosclerosis which is the main risk factor for stroke. B-cell maturation involves somatic hypermutation and genetic recombination generating antibody diversity. We specifically study the role of atypical chemokines in B-cell development in order to reveal their function in the development and induction of the somatic mutations.
Contact: Dr. Ozgun Gokce