Robert F. Niescier, Ph.D.
Postdoctoral Research Fellow
2018- present: Postdoctoral Research Fellow, Program in Neuroscience, Hussman Institute for Autism, Baltimore, MD
2017: Ph.D. Biomedical Sciences, Ulsan National Institute of Science and Technology, Republic of Korea
2009: B.S, Microbiology, University of the Sciences in Philadelphia
My previous research focused on the transport and function of mitochondria in neurons. Mitochondria are a ubiquitous organelle in eukaryotic organisms, responsible for aerobic energy production, calcium buffering, and apoptosis regulation. However, while these functions are required in most cell types, mitochondria are particularly vital in neuronal cells due to their significant energy requirement and polarized cellular structure. Mitochondria are required to be actively transported from the cell body to the far reaches of the axon, which can be several millimeters away from this structure. As a result, diseases that disrupt mitochondrial transport and function, such as Parkinson’s disease, frequently display profound neurological consequences.
Previous work examining mitochondrial movement has been hampered by the inherent limitations of live-cell microscopy, resulting in multiple discrepancies in the field. Using the photoswitchable protein Dendra2, we developed new techniques for analysis of movement of individual mitochondria across the whole axon. We found that mitochondria that enter the axon become independent from the cell body, and do not return for mitophagy or repair. Using this data, we were also able to mathematically model mitochondrial movement as a stochastic quality, which allowed for a more accurate analysis of mitochondrial velocity and movement patterns compared to conventional methods. This modeling technique allowed us to identify the mitochondrial calcium uniporter, or MCU, as a component of the mitochondrial transport machinery.
The NMDA receptor is a critical component of synaptic plasticity and signal transmission, and has been found to play a role in Autism Spectrum Condition (ASC). I am interested in exploring the molecular nature of this receptor in the context of Parvalbumin-expressing interneurons, which have been found to play an integral part in the formation and maintenance of neural networks, and whose downregulation has been found to induce symptoms found in ASC.
Niescier RF, Hong K, Park DG, & Min KT (2018) MCU interacts with Miro1 to modulate mitochondrial functions in neurons. Journal of Neuroscience 38(20):4666-4677. PMID: 29686046
Niescier RF, Kwak SK, Joo SH, Chang KT, & Min KT (2016) Dynamics of Mitochondrial Transport in Axons. Frontiers in cellular neuroscience 10:123. PMID: 27242435
Niescier RF, Chang KT, & Min KT (2013) Miro, MCU, and calcium: bridging our understanding of mitochondrial movement in axons. Frontiers in cellular neuroscience 7:148. PMID: 24058334
Chang KT, Niescier RF, & Min KT (2011) Mitochondrial matrix Ca2+ as an intrinsic signal regulating mitochondrial motility in axons. Proceedings of the National Academy of Sciences of the United States of America 108(37):15456-15461. PMID: 21876166