In the broadest sense, I am interested in how shape relates to function, and function dictates shape, in biological systems; let this be a protein, a cell, or a tissue.
In Tissue Mechanics Laboratory of LMCB, I am working on the mechanical regulation of tissue growth and shape formation. Understanding the regulation of tissue growth is of significant clinical interest, and can shed light on processes ranging from tissue regeneration, to inhibition of uncontrolled growth in cancer. Physical properties and mechanics are inherent to all biological processes, including emergence of tissue architecture. Yet, our tools to investigate mechanics, independent of biochemistry, are somewhere between limited to non-existent.
I am a computational biologist, and I am building computational models at cellular and tissue levels to investigate the roles of mechanics in growth and form. All computational models are developed in-house, using open source tools where necessary - with the core computations being in C++, and the simulation interface in Qt/OpenGL. In the long term, this will allow us to share our computational tools with the scientific community.
Within the Mao Lab in LMCB, I have access to cutting-edge experimental data for the model development, and we have the expertise to test our model predictions experimentally, both within the group, and within the LMCB community. Philosophically and financially, I am enjoying the support of Wellcome Trust in this project, with a Sir Henry Wellcome Postdoctoral Fellowship, and the biomechanics knowledge within LMCB, at both cellular and tissue levels.
My previous research focused on cell motility within the context of cancer, and cancer related mechanisms at the protein level. On cell motility, I have built a computational model to include actin polymerization and plasma membrane blebbing dependent cell motility mechanisms, and an explicit extracellular matrix (Tozluoğlu et. al. 2013). Using this model, we can predict the effects of biochemical perturbations in vivo, and we have shown that the geometry of the extracellular matrix alters the effective motility mode, and the response to interventions, in cancer cells.At protein-protein interaction (PPI) network level, I focused on construction and analysis of the PPI network of p73, homologue of tumour suppressor protein p53 (Tozluoğlu et. al. 2008). At direct protein-protein interaction level, with a Molecular-Dynamics approach, I investigated the mechanistic determinants of SUMOylation pathway, identifying allosteric regulation of SUMO E2 ligase Ubc9 via E3 ligase RanBP2 (Tozluoğlu et. al. 2010, Karaca et. al. 2011).