Dr. Yellajoshyula received his PhD in the Department of Biochemistry from the University of Mississippi Medical Center, where he studied the contributions of chromatin plasticity and linker histone, H1 in cell fate and development of embryonic and erythroid lineage in the laboratory of Dr. David Brown. He did his postdoctoral work at Washington University School of Medicine, St.Louis, where his studies in the lab of Dr. Kristen Kroll focused on the identification of transcriptional and epigenetic mechanisms controlling the transition from stem cell to neural fate. As a research faculty at the University of Michigan, Neurology, he has worked with Dr. William Dauer to develop mouse models for a commonly inherited form of dystonia, DYT6, to study mechanisms underlying dystonia pathogenesis. His studies have helped identify the role of oligodendrocyte lineage and myelination in dystonia pathogenesis.
Dr. Yellajoshyula’s work focuses on understanding the cellular and transcriptional mechanisms regulating the development of oligodendrocyte (OL), which are the glial cells in the CNS responsible for post-natal myelination of axons during development. His current research project focuses on elucidating the role of OL lineage in dystonia, a debilitating neurological movement disorder characterized by prolonged involuntary movements. One commonly-inherited form of dystonia, DYT6 is caused by mutations in the gene coding for THAP1, an atypical zinc finger transcription factor. Recent work has identified that THAP1 selectively affects the function of OL lineage in the developing CNS by regulating their development into mature cell-state, that is responsible for myelination. Mice lacking THAP1 or expressing a dystonia-causing missense allele selectively within OL exhibit strikingly delayed myelination. These studies complement DTI neuroimaging observations of white matter microstructural abnormalities in human DYT6 dystonia and add to the growing evidence of myelin abnormalities in inherited and idiopathic forms of dystonia. Together with an increasing appreciation for the role of myelin in neurodevelopmental disorders and plasticity, these findings suggest a largely uncharacterized role for OL lineage in dystonia pathogenesis.
Areas of Interest
Myelination, Oligodendrocyte, Movement disorders, Dystonia, THAP1.
Oligodendrocyte Development, Transcriptional Mechanisms of neurodevelopment and disease, Stem Cells, DYT6/THAP1.
- PhD, Biochemistry, University of Mississippi Medical Center, Jackson, MS, 2006
- MICHR-Organogenesis PTSP Scholar, Department of Neurology, University of Michigan 2012 – 2014