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development of the Enteric Nervous System


Using various lineage tracing and fate-mapping transgenic models, we study the development of the ENS during embryonic development, post-natal life, and in adulthood.

Our seminal discovery published in eLife in August 2023 is the first report of non-neuroectodermal and mesodermal derivation of neurons. This discovery, which reverses long standing dogma, has implications for post-natal maturation and aging of the ENS, as these mesoderm-derived enteric neurons (MENs) rapidly expand during juvenile period to attain proportional parity with the canonical neuronal lineage, and become the dominant neuronal lineage with age.

Our current and future work is focussed on understanding the developmental biology of MENgenesis.

rejuvenation of the aging Enteric Nervous System

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Using lineage fate mapping models, we show that the MENs originate in the post-natal gut and their rapid expansion during juvenile period drives post-natal development of ENS.

The culmination of this post-natal developmental process results in the MEN lineage becoming the dominant lineage of neurons in the gut - which is associated with dysfunction. We show that a growth factor mediated revitalization and rejuvenation of the ENS is possible to rescue function in the elderly.

Our current and future work is focussed on identifying the molecular and cellular factors responsible for this effect

MAINTENANCE of the Enteric Nervous System

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Previous dogma suggested a lack of steady state neurogenesis in the adult mammalian gut, leaving unanswered the question of how the adult ENS maintains itself, despite detectable neuronal loss.

In a pioneering work that we published in collaboration with the Pasricha Lab at JHU, we provided the first evidence of an active and rapid turnover of adult enteric neurons. By discovering the true identity of the Enteric Neural Stem Cells in adult gut, our team was the first to report on an active and a robust pathway of adult enteric neurogenesis.


Our work shows for the first time that the putative cause of gastrointestinal dysmotility is not neuronal deficits or dysfunctions but are pathological alterations in their precursor cells.

Our current work focuses on elucidating the cellular and molecular pathways that are associated with healthy neurogenesis, along with studying the biotic and abiotic factors that alter it causing gastrointestinal dysmotility.

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