UCONN

HEALTH

Photo of Yuanhao James  Li, Ph.D.

Yuanhao James Li, Ph.D.

Professor, Genetics and Genome Sciences
Academic Office Location:
Genetics and Genome Sciences
UConn Health
400 Farmington Avenue
Farmington, CT 06030-6403
Phone: 860-679-3836
Fax: 860-679-8345
Email: jali@uchc.edu
Website(s):

Genetics & Developmental Biology Graduate Program

Neuroscience Graduate Program

James Li Lab Page

Education
DegreeInstitutionMajor
B.S.Zhongshan UniversityBiochemistry
Ph.D.University of TexasMolecular Genetics

Post-Graduate Training
TrainingInstitutionSpecialty
PostdoctoralHHMI in Skirball Institute of Biomolecular Medicine, New York University School of MedicinePostdoctoral Fellow in the Developmental Genetics Program

Awards
Name of Award/HonorAwarding Organization
Individual National Research Service Award
Name & DescriptionCategoryRoleTypeScopeStart YearEnd Year
UCHC Biomedical Sciences graduate admissions committeeEducation CommitteeMemberUConn HealthUniversity20132016
Animal Services Advisory Committee of UCHCAdvisory CommitteeMemberUConn HealthUniversity2007
UCHC Biomedical Sciences Graduate Admissions CommitteeAdvisory CommitteeMemberUConn HealthUniversity20052007
Society for Developmental BiologyProfessional/Scientific OrganizationMemberExternalNational
Society for NeuroscienceProfessional/Scientific OrganizationMemberExternalNational

Research Interest My lab investigates how different brain cells, neurons and glia, are generated from neural stem cells and how brain cells form the neuronal network. These questions are fundamentally important to understand brain development. Knowledge of the developmental events will provide insight into the molecular and cellular mechanisms that underpin neurological diseases, such as Parkinson’s disease, autism, schizophrenia and depression. We combine several molecular and cellular approaches, including mouse genetics, in vitro assays, genomics, developmental neuroanatomy, and embryonic stem cells in our studies. Our on-going projects focus on two embryonic brain regions, the diencephalon (thalamus and habenular) and the mes-metencephalon (midbrain and cerebellum).


Molecular mechanisms of differentiation of habenular and thalamic neurons The thalamus and the associated habenula are derived from closely related progenitor domains. They together play important roles in modulating sensory, motor, cognitive and emotive functions. Habenular neurons receive inputs from the limbic system, and in turn connect and modulate the dopamine and serotonin systems of the midbrain and hindbrain. By contrast, thalamic neurons receive peripheral sensory inputs and project rostrally to the cortex. Abnormal formation and function of the habenula and thalamus have been implicated in brains disorders, such as depression, schizophrenia, sleeping disorders, and epilepsy. We recently identify key molecules that regulate the differentiation between habenular and thalamic neurons. Our long-term goal is to determine the molecular mechanisms that regulate thalamic and habenular identities and connectivities. Ultimately, this information will facilitate understanding the brain disorders resulting from abnormal formation and/or function of the thalamus and habenula.


Radial glial development in the cerebellum During cortical development of the cerebrum and cerebellum, radial glia cells in the ventricular zone provide guidance for neuronal migration and serve as stem cells for neurons and glial cells. Therefore, radial glial development is crucial for the formation of normal cortical architectonics. In contrast to the transient appearance of radial glia in the neocortex, cerebellar radial glia transform into specialized radial glia-like cells, called Bergmann glia. Bergmann glia maintain only the long basal processes and persist throughout the life of the animal. During cerebellar development, the Bergmann glial fibers provide scaffolds for migratory neurons. Interestingly, in both immature and mature cerebellum, Bergmann glia display hallmarks of neural stem cells. We recently discover the first known genetic mutation that specifically blocks Bergmann glial generation in mice. Analyses of the mutant mice also uncover a previously unappreciated function of Bergmann glia in the morphogenesis of the cerebellar cortex. Using whole genome transcriptome analysis, we identify putative genetic determinants for Bergmann glial generation. Remarkably, many of these Bergmann glia-specific genes have been implicated in the malignancy of glioma and medulloblastoma in adults and children, the most common primary malignant brain tumors in adults and children. These exciting findings will allow us to define the molecular and cellular mechanisms controlling Bergmann glial generation in the developing cerebellum. The acquired information would shed light on the molecular pathways leading to tumorigenesis in the brain.

Accepting students for Lab Rotations: Summer '17, Fall '17, Spring '18


 

Journal Articles

Title or AbstractTypeSponsor/EventDate/YearLocation
Bergmann Glia Development, Genesis and DifferentiationTalkThe 8th International Symposium of the Society for Research on the Cerebell2017Winnipeg, Manitoba , Canada
Shp2-dependent ERK signaling is essential for induction of Bergmann glia and foliation of the cerebellumPanel Discussion2014Ventura, CA
Analysis of the development of the mouse inner ear using Gbx2 as a guide.PosterSociety for Neuroscience Annual Meeting2008Washington, DC
Cassette Exchange”: a Cre-loxP mediated recombination method for efficient generation of stable transgenic human embryonic stem cell lines.PosterAnnual Connecticut Stem Cell Technology Symposium2008Farmington, CT
Gbx2-dependent program regulates axon guidance of the thalamocortical projections. PosterGordon Conference on Neural Development2008Newport, RI
Gbx2 and Fgf8 are sequentially required for formation of the mid-hindbrain compartment boundary.PosterSociety For Developmental Biology, 67st Annual Meeting2008Philadelphia, PA
Gbx2-dependent program regulates axon guidance of the thalamocortical projections.PosterNortheast Regional Developmental Biology Meeting2007Northeast, USA
Fgf8 function is orchestrated by different Fgf8 splice variants.PosterGordon Conference on Fibroblast, Growth Factors In Development & Disease2006Ventura, CA
Fgf8 function is orchestrated by different Fgf8 splice variants.PosterDevelopment Biology, Gordon Research Conferences2005New Hampshire
Expressing Gbx2 in rhombomere 4 in Gbx2 mutants rescues rhombomere 3 and causes deletion of the posterior midbrain.PosterDevelopment Biology, Gordon Research Conferences2003New Hampshire
Temporal requirements for Gbx2 in cerebellar development. PosterSociety For Developmental Biology, 61st Annual Meeting2002New Hampshire
Genetic analysis of Otx2 and Gbx2 function in mid-hindbrain development.Poster2001 Development Biology, Gordon Research Conferences2001New Hampshire