Sample Research Statement-3

Academic Statement of Purpose/Research Statement
Bivas Nag
I have a long-standing interest in brain development. Through my previous research

experiences described below, I have focused on working toward gaining skills important for
becoming a neuroscientist.
During my undergraduate studies at St. Xavier's Mumbai, I joined Dr. Shubha Tole's laboratory
to learn about forebrain development. I was involved in a project studying the establishment of
connectivity between the thalamus and the cortex, focused on the role of Lhx2 in cortical
progenitors on later cortical patterning. Using immunofluorescence, in-situ hybridization, and
viral tracing, we showed that the loss of Lhx2 specifically disrupts the waiting phase of
thalamocortical axons, resulting in aberrant barrel cortex formation and the loss of appropriate
sensory connections. I was curious whether the early deletion of Lhx2 from the cortical
progenitor has an effect on the thalamus. My experiments showed atrophy of the sensory
nucleus at later point. I presented this work at various conferences and received the DD
Kosambi Young Scientist Award, KS Krishnan Mentor Award, and SK Mahajan Award for
Popularisation of Scientific Pursuits.
Afterward, I moved to Munich to join Ludwig Maximilian University (LMU) for my master’s
degree in Molecular and Cellular Biology. In my first rotation in Dr. Magdalena Gotz’s lab, I
joined a project focused on analyzing changes in the neurovascular unit in the dentate gyrus of
the age-based Alzheimer’s Disease (AD) mice model. My role in the project was to optimize
iterative indirect immunofluorescence imaging (4i) on mouse tissue to study the stem cell niche
with a neurovascular unit. Our work showed that the permeability of the neurovascular unit
influences adult neurogenesis and becomes more pronounced in AD and aging.
For my second rotation, I joined Dr. David Keay's laboratory and led a project investigating the
role of mutations in microtubule-associated proteins on cortex development. This project was
built on mass spectrometry data identifying protein enriched in the cortex of genetically modified
mice with the R402H mutation in the TUBA1 gene, We studied the mutations in these proteins
and their influence on cortex development using molecular biology techniques such as cloning
and western blotting, and cell culture techniques to study neuron and organoid cultures. I
presented my data at the Neuroscience Retreat at the University of Cambridge.
My final rotation was in the laboratory of Dr. Gunnar Schotta, where I learned about the
potential of genomic approaches in neuroscience. I worked on epigenetic silencing mechanisms
of endogenous retroviruses(ERVs). Previous research suggested that Setdb-1 mediated
H3K9me3 is not sufficient to silence ERVs. My study showed the role of the gene Cfdp1 in
enhancing Setdb1-mediated methylation. I generated CRISPR knockouts of Cfdp1 in embryonic
cell lines and used CUT&TAG and ATAC-seq to study changes in chromatin accessibility. I
showed that overall methylation patterns decreased after Cfdp1 deletion. I also investigated the
interplay between Morc3-Daxx-Atrx in the deposition of a histone variant (H3.3), which
additional silences ERVs. I also created a Morc3-flagged construct to transfect it in Atrx and
DaxxKO cell lines to do a ChIP-MS experiment to understand Morc3's involvement in the
turnover of histone H3.3. These experiences helped me develop the skills to design
experiments independently and formulate focused hypotheses.
For my master's thesis, I moved to the United States to join Dr. Kartik Pattabiraman's laboratory
in collaboration with Dr. Nenad Sestan at Yale University. I spearheaded a project to
characterize the genetic landscape of neuropsychiatric disorders by characterizing the binding
patterns of DNA binding proteins associated with psychiatric disorders. We hypothesized there
would be an enrichment of human or primate-specific binding sites in non-coding regions of
genomes associated with these disorders. Over the first several months, I optimized CUT &
RUN and ChIP-seq pipelines for different transcription factors in both mouse and human tissues
to identify signal-to-noise better and increase reproducibility. Given the extended timeline
necessary for data generation, sequencing, and subsequent analysis, I took the initiative to
learn the analysis phase to expedite the process and bring the analysis in-house. I also used an
orthogonal approach of electroporating tagged versions of transcription factors into the mouse
prefrontal cortex to enhance the efficiency of the experiments. I am also collaborating with
members of the Sestan Lab to characterize conserved and species-specific components of the
retinoic acid-dependent gene regulatory network active in the prefrontal cortex.
I applied the computational skills I learned from previous projects to assist with other ongoing
projects in the Pattabiraman lab. 22q11 deletion syndrome (DS) is one of the strongest known
single genetic risk factors for schizophrenia and has been associated with abnormal
development and aberrant subcortical connectivity. I analyzed RNA-seq data and diffusion
tensor imaging generated to characterize the developmental trajectory of the mouse model of
22q11DS. I utilized my growing skills to assist other lab members and contributed to the grant
writing process. Altogether, my position at Yale has allowed me to conduct research full-time; I
have a sense of what graduate school will be like strengthening my desire to pursue a Ph.D.
As I move forward, I want to find the molecular and cellular uniqueness underlying the human
brain and explore how these findings can help us enhance our understanding of various
psychiatric disorders. My research interests closely align with the work of several neuroscience
faculty members, such as Dr. Ken Kwan and Dr. Stephanie Bielas, who investigate the genetic
basis and evolutionary aspects of human brain development and vulnerabilities. I am particularly
interested in exploring cross-species evolutionary patterns using cutting-edge single-cell
genomics techniques. Additionally, the research conducted by Dr. Shigeki Iwase on chromatin
regulatory mechanisms and their role in brain development is also fascinating. I am also
intrigued by the work of Dr. Louis Dang on understanding the pathophysiology of genetic causes
of different neuropsychiatric disorders. I could see myself integrating well into any of these labs
and the Neuroscience program at Michigan.
Michigan’s impressive array of cross-disciplinary research offers me an ideal platform to

leverage my previous experiences to contribute to the field effectively. The department's diverse
cohort and experienced mentors will help me prepare for my future goal of becoming a principal
investigator focused on brain evolution and development. My drive and relentless pursuit of
knowledge, coupled with my skills and ambitions, will position me to thrive in the graduate
program at Michigan.

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Sample Research Statement-3

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Academic Statement of Purpose/Research Statement

I have a long-standing interest in brain development. Through my previous research

Michigan’s impressive array of cross-disciplinary research offers me an ideal platform to

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