Dr. Hobert is also a professor of biochemistry and molecular biophysics at Columbia University Medical Center and a professor of biological sciences at Columbia University.
Oliver Hobert studies molecular mechanisms that control the generation of the enormous diversity of cell types in the nervous system. Using Caenorhabditis elegans as a model system, his laboratory decodes genomic cis-regulatory information of gene batteries expressed in specific neuronal cell types and identifies trans-acting factors that act at various stages of neuronal development to impose specific terminal differentiation programs onto individual neuron types.
Oliver Hobert obtained his diploma in biochemistry at the University of Bayreuth, Germany, in 1992 and his Ph.D. in molecular biology at the Max Planck Institute for Biochemistry in Munich in 1995. Fascinated by the experimental amenability of the model system Caenorhabditis elegans, Hobert joined Gary Ruvkun's lab at Harvard Medical School for postdoctoral research. Studies on the function of several transcription factors allowed him to define his long-term research interest in how neurons in the nervous system are genetically programmed during development.
In 1999, Hobert took a faculty position in the Department of Biochemistry and Molecular Biophysics at Columbia University College of Physicians and Surgeons, where he continued to pursue and expand his research interest in nervous system development. While studying when and where genes act during the development of the C. elegans nervous system, Hobert discovered a new phenomenon that he has termed axon maintenance. He showed that axonal positioning is not determined once and for all, as many had thought, but must be actively maintained. After the developing body lays down the wiring pattern for the nervous system, certain proteins are responsible for maintaining that architecture. This surprising conclusion emerged through Hobert's identification of a family of six proteins called ZIGs. Loss of zig gene activity causes "flip-over" defects, a failure of axons to be maintained in their correct positions in defined bundles.
Hobert has proposed that this maintenance mechanism exists to enable axons to withstand mechanical stress and changing environments during growth—circumstances that are not only relevant to C. elegans but also may be directly applicable to the vertebrate nervous system.
Hobert's other main interest lies in understanding how cell fate diversity is created in the nervous system. Specifically, he has contributed to understanding how the developing C. elegans nervous system establishes cellular diversity along the left-right axis. By dissecting a pathway that controls left-right asymmetry of the ASE chemosensory neurons, involved in taste response, Hobert has defined a set of proteins responsible for the left-right patterning of these neurons. Recently he made the striking discovery that small bits of RNA, or microRNAs, function as their key regulators. These studies may provide clues to the molecular machinery driving differences between the left and right sides of the human brain.