Sergey Ovchinnikov uses phylogenetic inference, protein structure prediction/determination, protein design, deep learning, energy-based models, and differentiable programming to tackle evolutionary questions at environmental, organismal, genomic, structural, and molecular scales, with the aim of developing a unified model of protein evolution.
Ferroptosis is an iron-dependent form of cell death with profound implications in human health and disease. In the context of cancer, the use of ferroptosis inducers to target subpopulations of highly metastatic and therapy-resistant cancer cells has garnered much excitement over the last few years. However, to gain a comprehensive understanding of the full therapeutic potential of ferroptosis, our research focuses on (i) uncovering the molecular factors affecting ferroptosis susceptibility, (ii) studying its impact on the tumor microenvironment, and (iii) developing innovative ways to modulate ferroptosis resistance in vivo. We employ a multidisciplinary approach, combining functional genomics, metabolomics, bioengineering, and a range of in vitro and in vivo models to advance our understanding in this domain and to translate our findings into effective therapies.
B lymphocytes are the fulcrum of our immunological memory, the source of antibodies, and the focus of vaccine development. My lab has investigated how, where, and when B cell responses take shape. In recent years, my group has expanded into preclinical vaccinology, developing cutting-edge humanized mouse models for diseases including malaria, HIV, and SARS-CoV-2.
Different cells take on an astonishing variety of shapes, which are often critical to be able to perform specialized cell functions like absorbing nutrients or contracting muscles. We study how different cell shapes arise and how cells control the spatial distribution of their internal constituents. We take advantage of the tractability of fungal model systems, and address these questions using approaches from cell biology, genetics, and computational biology to understand molecular mechanisms.
Sally Kornbluth is President of MIT. Before she closed her lab to focus on administration, her research focused on the biological signals that tell a cell to start dividing or to self-destruct — processes that are key to understanding cancer as well as various degenerative disorders. She has published extensively on cell proliferation and programmed cell death, studying both phenomena in a variety of organisms. Her research has helped to show how cancer cells evade this programmed death, or apoptosis, and how metabolism regulates the cell death process; her work has also clarified the role of apoptosis in regulating the duration of female fertility in vertebrates.
We use the tiny, transparent jellyfish, Clytia hemisphaerica, to ask questions at the interface of nervous system evolution, development, regeneration, and function. Our foundation is in systems neuroscience, where we use genetic and optical techniques to examine how behavior arises from the activity of networks of neurons. Building from this work, we investigate how the Clytia nervous system is so robust, both to the constant integration of newborn neurons and following large-scale injury. Lastly, we use Clytia’s evolutionary position to study principles of nervous system evolution and make inferences about the ultimate origins of nervous systems.
Diverse commensal microbes colonize every surface of our bodies. We study the constant communication between these microbes and our immune system. We focus on our largest organ: the skin. By employing microbial genetics, immunologic approaches, and mouse models, we can dissect (1) the molecular signals used by microbes to educate our immune system and (2) how different microbial communities alter immune responses. Ultimately, we aim to harness these microbe-host interactions to engineer novel vaccines and therapeutics for human disease.