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I'm a graduate student at UC Berkeley in the Department of Molecular and Cell Biology.
I'm interested in the use of self-patterning organoids to recapitulate developmental events unique to humans and to model complex tissue architecture. I have training in stem cell biology, 2D and 3D culture systems, molecular biology, and bioinformatics.
Learn more about me below:
Education & Training
Education
Academic
University of California, Berkeley
Ph.D. (in progress), Molecular and Cell Biology
2022 - present
Tufts University
M.S., Biology (Genetics, Molecular and Developmental Biology)
2018 - 2020
Brown University
Sc.B. (Honors), Neuroscience
2008 - 2012
Training
Research Appointments
Graduate Student Researcher (GSR)@ University of California, Berkeley
Present
I'm studying the role of cardiac neural crest cells in the the human heart using hiPSC and hESC-derived cardiac organoids (cardioids).
Neural crest cells, a migratory population of cell, comes into an otherwise majority mesoderm-derived tissue during development
to form structures such as major arteries, septa, and valves. They also differentiate into a small subset of cardiomyocytes.
Cardiomyocytes derived from this stem cell population have been shown to respond to injury in teleost fish —
de-differentiating, proliferating, and re-differentiating to reform the lost tissue. I'm studying the gene regulatory networks
that govern this species-specific regenerative process in a human cardioid/NCC co-culture system that I am developing, multiomics,
and CRISPRa/i.
Fulbright Research Fellow@ Institute of Molecular Biotechnology - Austrian Academy of Sciences (IMBA)
Mar 2021 - Aug 2022
I worked with cerebral organoids (three-dimensional tissues that model the core cellular makeup and cytoarchitecture of the
brain) to study the role of exogenous and endogenous extracellular matrix (ECM) in dorsal-ventral patterning, polarization of
the neuroepithelium and neural rosette, generation of proper cortical cytoarchitecture, and specification of different cell
populations.
I also used cerebral organoids to examine how haploinsufficiency of ARID1B, a subunit of the SWI/SNF chromatin remodeling complex, can lead to abnormal development of callosal projection neurons (CPN) and to corpus callosum agenesis. We uncovered abnormal axonal pathfinding and impaired axonogenesis in various mutants of ARID1B.
I also used cerebral organoids to examine how haploinsufficiency of ARID1B, a subunit of the SWI/SNF chromatin remodeling complex, can lead to abnormal development of callosal projection neurons (CPN) and to corpus callosum agenesis. We uncovered abnormal axonal pathfinding and impaired axonogenesis in various mutants of ARID1B.
Research Associate@ Massachusetts Institute of Technology (MIT)
Sep 2016 - Mar 2021
I worked with cerebral organoids to elucidate early neurodevelopmental deficits that arise in autism spectrum disorders, specifically in the X-linked disorder Rett Syndrome (RTT). In organoids produced from Rett patient-derived induced pluripotent stem cells (iPSCs) harboring either mutant MeCP2 or their respective isogenic wild-type copy (obtained from X-inactivated clones or gene editing), we showed that MeCP2 deficiency was associated with an increase in neural progenitor proliferation and concomitant decrease in neurogenesis and neuronal migration and maturation. This phenotype was due to dysregulation of the AKT/ERK pathway. My project was to further investigate the molecular mechanism of this migration deficit. Using proteomic techniques, I found an increase in GSK3β/β-catenin signaling, downstream of AKT, in RTT organoids. Using multi-photon and confocal microscopy of virally labeled and immunostained organoids, I also found that, although the morphology and polarity of radial glial cells are mostly preserved, adhesion molecules were dysregulated and neuronal migration trajectory and speed were disrupted in MeCP2-mutant organoids.
Research Assistant@ Massachusetts General Hospital/Harvard Medical School (MGH/HMS)
Sep 2013 - Sep 2016
I studied the protein dynamin and its interactions with actin and other scaffolding proteins. IS discovered that when dynamin was promoted to oligomerize into higher-order structures, it was protected from cleavage by calpain, a protease associated with dendritic pruning. Through confocal and electron microscopy, I then demonstrated that these dynamin oligomers can influence the architecture of the actin cytoskeleton by both stimulating actin polymerization and crosslinking/bundling actin filaments. I also demonstrated through biochemical assays that this stimulation was direct, as genetic manipulation of cytoskeletal adaptor proteins had no effect on the ability of dynamin oligomers to influence the actin cytoskeleton. Finally, to bridge cell structure to cell function, I examined what effect different dynamin mutants and dysregulated cytoskeletal dynamics had on not just endocytosis and intracellular trafficking (canonical roles of dynamin) but also cell adhesion and migration.
Research Assistant@ Brown University
May 2011 - Aug 2013
Because calcium can mediate a diversity of cellular responses, cells prevent off-target effects by utilizing the duration, localization, and magnitude of calcium signals to specify certain outcomes. My project was to resolve the paradoxical observation that some classes of Sigma-2 (σ2) Receptor ligands could lead to cell death while others lead to cell proliferation. Through pharmacological manipulation and calcium imaging, I discovered that σ2R activation induced changes in sphingolipid metabolism, which, in turn, encoded different phasic calcium signatures. Therefore, depending on the kinetics and binding affinities of the ligand, there can be a metabolic shift to either a family of sphingolipids that produced a transient rise in calcium responsible for cell growth or to another family of sphingolipids that produced a latent and sustained rise in calcium responsible for cell death/apoptosis.