Jayshree Samanta, MBBS, PhD
Position title: Assistant Professor, Department of Comparative Biosciences
Visit the Samanta Lab
Our lab focuses on how neural stem cells generate myelin in the brain during development as well as during recovery from a demyelinating insult i.e. remyelination. Our primary goal is to understand the disease process and identify factors that can help neural stem cells repair the brains with myelin abnormalities, including Down Syndrome and Multiple Sclerosis.
The myelin sheath is a specialized membrane synthesized by oligodendrocytes, which wraps around the axons of neurons in the vertebrate brain. In demyelinating diseases, disruption of myelin results in severe neurological defects due to conduction block ultimately leading to the loss of axons. The goal in inherited myelin diseases is to myelinate axons that have not been ensheathed; while in demyelinating diseases, the goal is to ensheath the axons that have lost their myelin. Our objective is to understand the molecular underpinnings of signaling pathways with respect to their role in proliferation, migration and differentiation of neural stem cells during developmental myelination and remyelination.
We use several techniques to study myelin generation from neural stem cells:
1. Mouse models of diseases: To study remyelination, we induce demyelination in the brain with Lysolecithin injection, Cuprizone diet or use genetically modified mice responsive to Diphtheria toxin. We also use genetic models recapitulating human Trisomy 21 to study Down Syndrome in mice.
2. In vivo mouse genetics: We label specific populations of neural stem cells in the brain using genetically inducible fate-mapping techniques like Cre-Lox recombination. We also use genetically modified mice to activate or inhibit specific signaling pathways in neural stem cells by overexpressing or ablating different components of the pathway.
3. In vitro neural stem cell culture: We harvest neural stem cells from the ganglionic eminences in embryonic brains and subventricular zone in adult mouse brains and grow them as suspension cultures in a dish. In addition, we manipulate the signaling pathways pharmacologically or genetically to study proliferation and differentiation of neural stem cells in vitro.
- Daniel Z. Radecki*, Heather Messling*, James R. Haggerty-Skeans, Jayshree Samanta**, James L. Salzer** (2019). Gli2 is necessary for migration of ventral Neural Stem Cells to demyelinated lesions. bioRxiv 668418; doi: https://doi.org/10.1101/668418. *,** Equal contribution
- Samanta J, Grund EM, Silva HM, Lafaille JJ, Fishell G and Salzer JL (2015). Inhibition of Gli1 mobilizes endogenous neural stem cells for remyelination. Nature, 526: 448-452
- Samanta J*, Alden T*, Gobeske K, Kan L and Kessler JA (2010). Noggin protects against ischemic brain injury in rodents. Stroke 41(2): 357-362. *Equal contribution.
- Samanta J, Burke GM, McGuire T, Pisarek AJ, Mukhopadhyay A, Mishina Y and Kessler JA (2007). Bmpr1a signaling determines numbers of oligodendrocytes and Calbindin-expressing interneurons in the cortex. Journal of Neuroscience 27(28): 7397-7407.
- Samanta J and Kessler JA (2004). Interactions between ID and OLIG proteins mediate the inhibitory effects of BMP4 on oligodendroglial differentiation. Development 131(17): 4131- 4142.