Developmental neurobiology · gene regulation · data science
Manni Adam
I study brain development as a problem of regulatory coordination: how chromatin, transcription, RNA processing, and protein-level systems act across developmental time to shape cell fate, and how disruption of that coordination contributes to neurodevelopmental disease.
- Focus
- Gene regulation in brain development
- Systems
- Chromatin · RNA · protein networks
- Approach
- Multiomic, lineage-resolved, computational
About
Bridging brain development, molecular mechanisms, and data.
Hello, I’m a developmental neurobiologist and postdoctoral fellow in the Harwell Lab at UCSF. My research asks how gene regulatory systems build the brain, with a focus on how chromatin state, transcription, RNA processing, and protein-level regulation coordinate cell-state transitions during development.
I completed my PhD at the MRC Centre for Neuropsychiatric Genetics and Genomics at Cardiff University, after earning an MSc in Neuroscience with a focus on Developmental Neurobiology at King’s College London and an undergraduate degree in Biological Sciences from Bournemouth University.
My work combines developmental neurobiology, regulatory genomics, long-read sequencing, proteomics, lineage and trajectory analysis, and computational integration to identify vulnerable cell states, developmental windows, and regulatory nodes in neurodevelopmental disease.
Research questions
Questions I’m drawn to
My research program is organized around three linked problems: how regulatory layers cooperate, how developmental states carry information across time, and why diverse perturbations converge on shared neurodevelopmental disease mechanisms.
How do regulatory layers cooperate to control cell fate?
Brain development depends on timed transitions through progenitor and postmitotic states. I study how chromatin accessibility, transcription, RNA processing, and protein interactions coordinate to establish regulatory potential, execute fate decisions, and stabilize identity.
Principle: cell fate is an emergent outcome of coordinated regulatory systems, not isolated molecular events.
How are transient developmental states encoded across time?
Many decisive developmental states are short-lived, but their molecular features can shape later neuronal and glial identity, maturation, and function. I use temporal and lineage-resolved approaches to connect early progenitor states with later outcomes.
Principle: developmental mechanisms need to be studied as trajectories, not static snapshots.
How do diverse perturbations converge on shared disease mechanisms?
Autism and intellectual disability are genetically heterogeneous, yet they often share molecular, cellular, and developmental features. I investigate how disruption of chromatin modifiers, transcriptional programs, RNA processing, protein complexes, or developmental timing can converge on common vulnerabilities.
Principle: neurodevelopmental disease can be understood as a failure of regulatory coordination.
Approaches
Linking regulatory state, molecular mechanism, and developmental outcome.
My research integrates experimental and computational approaches to understand how gene regulatory systems are coordinated during brain development. I combine cell-resolved genomics, chromatin profiling, transcriptomics, long-read sequencing, perturbation, proteomics, and cross-species analysis to connect molecular mechanisms with cell fate, maturation, and neurodevelopmental disease risk.
Multi-layer regulatory genomics
I use complementary genomic approaches to define how regulatory state changes across developmental time, from chromatin accessibility and transcription factor-associated chromatin programs to transcriptional output, RNA processing, and cell identity.
- ATAC-seq, CUT&RUN, ChIP-seq, RNA-seq, cell-resolved profiling, and long-read sequencing
- Integration of chromatin state, gene expression, transcript structure, and developmental identity
- Analysis of cell-type- and stage-specific regulatory programs during brain development
Lineage-resolved fate mapping
I use lineage- and stage-resolved strategies to understand how regulatory programs shape progenitor competence, temporal fate transitions, and the production of neuronal and glial cell types. This approach links enhancer repertoires and chromatin state to developmental outcome.
- Profiling regulatory programs across defined progenitor, transitional, and differentiated cell states
- Trajectory analysis linking progenitor programs to differentiated cell states
- Linking transient regulatory states to later cell identity, maturation, and fate specification
Functional testing of regulatory mechanisms
I use perturbation-based approaches to move from regulatory maps to causal mechanism. Candidate enhancers, noncoding regions, transcriptional regulators, and chromatin-modifying pathways can be tested for their roles in cell-state transitions and developmental outcomes.
- CRISPR/dCas9-based perturbation of regulatory elements and gene programs
- Targeted epigenome-engineering strategies to test chromatin-state function at candidate loci
- Functional interrogation of enhancers, noncoding regions, and disease-associated regulatory mechanisms
Integrative mechanism discovery
I combine computational analysis with experimental discovery to identify the regulatory networks and molecular complexes that coordinate neurodevelopment. This includes integrating genomic, transcriptomic, long-read, lineage-resolved, and proximity-based proteomic datasets across complementary projects.
- Computational integration across regulatory genomics, transcriptomics, long-read, and proteomic datasets
- Proximity-based proteomics to identify protein interactions and regulatory complexes
- Comparative analysis of mouse and human systems to define conserved and disease-relevant regulatory logic
Education
Degrees earned.
Cardiff University
PhD in Neuroscience
King’s College London
MSc Neuroscience in Developmental Neurobiology · Distinction
Bournemouth University
BSc Biological Sciences · First Class Honours
Publications
Selected publications
Temporal and sequential transcriptional dynamics define lineage shifts in corticogenesis
Mukhtar, T.; Breda, J.; Adam, M. A.; et al. (2022). The EMBO Journal 41(24): e111132.
Transcriptional profiling of sequentially generated septal neuron fates
Turrero García, M.; Stegmann, S. K.; Lacey, T. E.; Reid, C. M.; Hrvatin, S.; Weinreb, C.; Adam, M. A.; Nagy, M. A.; Harwell, C. C. (2021). eLife 10: e71545.
Transcriptional regulation of MGE progenitor proliferation by PRDM16 controls cortical GABAergic interneuron production
Turrero García, M.; Baizabal, J. M.; Tran, D. N.; Peixoto, R.; Wang, W.; Xie, Y.; Adam, M. A.; et al. (2020). Development 147: dev187526.
Epigenetic regulation of cortical neurogenesis; orchestrating fate switches at the right time and place
Adam, M. A. and Harwell, C. C. (2020). Current Opinion in Neurobiology 63: 146–153.
EHMT1/GLP; biochemical function and association with brain disorders
Adam, M. A. and Isles, A. R. (2017). Epigenomes 1(3), article number 15.
Curriculum vitae
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