Research program
Schizophrenia and bipolar disorder each involve dozens of genetically distinct risk genes, but a mechanism tied to one rare mutation may have limited therapeutic reach—one shared across independent forms of genetic risk is likely to be more broadly useful. My research is built on that bet: that mapping how diverse risk genes converge on common molecular mechanisms, validated across genetic mouse models and human brain tissue, is the fastest route to therapeutically tractable biology. RNA regulation in the brain — translation, alternative splicing, and isoform control — is my primary lens onto this convergence, since disruption of these pathways recurs across several of the models I study.
Convergent mechanisms across psychiatric risk genes
I lead comparative analyses across genetic mouse models of schizophrenia and bipolar disorder, integrating synaptic proteomics, transcriptomics, and human brain datasets to identify molecular pathways that recur across distinct forms of genetic risk — the shared biology most likely to translate into therapeutic targets.
RNA regulation as a lens on convergence
RNA regulation is where I pursue this convergence question directly: I investigate how disruption of RNA-binding and regulatory proteins alters splicing, isoform expression, translation, and synaptic protein composition. Work on SRRM2 haploinsufficiency has shown how disruption of a single RNA splicing factor can produce coordinated isoform-specific, synaptic, and cellular abnormalities, including SynGAP-γ loss, Agap3 mis-splicing, and oligodendrocyte deficits.
From multi-omics signatures to mechanism
I use molecular, cellular, and functional experiments to test hypotheses emerging from large-scale datasets, connecting disease-associated molecular signatures to specific mechanisms and tractable intervention points. I am also investigating biomarkers such as NPTX2 that may report shared changes in neuronal activity and synaptic function across models and human disease.
Graduate research
Center for Neural Science, New York University
2014 – 2020
Ph.D. with Eric Klann, Ph.D.
- Led studies of dysregulated mRNA translation in fragile X syndrome using genome-wide ribosome profiling and cell-type–specific TRAP-Seq.
- Discovered alterations in translation efficiency in fragile X mouse brain and identified increased ribosome elongation as a key mechanism underlying translational dysregulation.
- Found that genetic reduction of the translational regulator S6K1 restores translational homeostasis and corrects synaptic and behavioral phenotypes in fragile X model mice.
- Contributed to collaborative studies linking altered translational control to cortico-striatal circuit dysfunction and repetitive behaviors.
As part of this earlier work on data analysis methods, I contributed to
DABEST, an open-source library for estimation graphics — visualizing effect sizes and their uncertainty as an alternative to p-value-only reporting (Ho, Tumkaya, Aryal, Choi & Claridge-Chang,
Nature Methods, 2019).
Core expertise
Multi-omics integration
Synaptic proteomics, network biology (WGCNA), cross-species meta-analysis
Functional genomics
Single-nucleus and bulk RNA-seq, ribosome profiling, TRAP-Seq
RNA regulation in the brain
Alternative splicing, mRNA translation, post-transcriptional regulation
Computational biology
Python, R, MATLAB, Bash; scalable analysis pipelines; HPC (Slurm/SGE)
Experimental neuroscience
Molecular biology, biochemical purification, imaging, CRISPR/Cas9, mouse genetics, AAV vectors
Scientific leadership
Supervision of research associates, coordination of cross-disciplinary research projects