Assistant Professor

Contact

badamson@princeton.edu
781.640.6444
Icahn Laboratory, 144

Faculty Assistant

Dawn Capizzi

Education

Ph.D. Genetics and Genomics, Harvard University
B.S., Biology, Massachusetts Institute of Technology

Research Area

Genetics & Genomics

Research Focus

The organization of cellular stress response networks and repair mechanisms

Website

Adamson Lab




Research
Selected Publications
Biography
Honors & Awards
The Adamson lab studies the organization and function of molecular networks in human cells, with particular focus on understanding (a) how cells differentially leverage these networks to respond to stress and (b) how abnormal programs of stress response contribute to disease. We also develop and improve innovative technologies for genetics and cell biology, including those with potential therapeutic applications such as genome editing.
Stress response networks have traditionally been studied in bulk assays and thus have been described largely as dedicated pathways with stereotyped activation regimes. However, we know that these systems are deeply complex, with diverse sensory mechanisms and integrated subroutines controlling cell outcomes. This complexity helps maintain normal cell function in response to diverse perturbations. Problematically, it can also allow cells to survive pathogenic network dysregulation or enable abnormal adaptation to multicellular disease states. Therefore, understanding stress responses at a systems-level and from a functional perspective is critical. We use and develop innovative experimental technologies, including CRISPR-based functional genomics, single-cell RNA-sequencing, and genetic interaction mapping, to investigate molecular and genetic networks. These high-resolution techniques allow systematic mapping of network behavior across conditions. From this, we identify interesting behaviors, with special interest in context-dependent behaviors, and then, using more conventional genetics and cell biology approaches, characterize underlying mechanisms. Current efforts include investigating how cells mount tailored responses to endoplasmic reticulum stress and DNA damage.
Genome editing technologies that target programmable sequence changes to specific genomic loci have substantial potential for therapeutic applications. However, realizing the promise of these approaches will require improving their to-date limited specificity. We have recently pioneered methods to systematically investigate how synthetic mechanisms of genome editing, including CRISPR-based single-strand template repair and DNA base editing, interact with endogenous DNA repair networks. One goal of this work is to identify parameters that can be tuned to achieve optimal in vitro and in vivo editing outcomes.




Koblan LW, Arbab M, Shen MW, Hussmann JA, Anzalone AV, Doman JL, et al. Efficient C?G-to-G?C base editors developed using CRISPRi screens, target-library analysis, and machine learning. Nat Biotechnol. 2021 ;39(11):1414-1425. PubMed
BibTex

Chen PJ, Hussmann JA, Yan J, Knipping F, Ravisankar P, Chen P-F, et al. Enhanced prime editing systems by manipulating cellular determinants of editing outcomes. Cell. 2021 ;184(22):5635-5652.e29. PubMed
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Hussmann JA, Ling J, Ravisankar P, Yan J, Cirincione A, Xu A, et al. Mapping the genetic landscape of DNA double-strand break repair. Cell. 2021 ;184(22):5653-5669.e25. PubMed
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Replogle JM, Norman TM, Xu A, Hussmann JA, Chen J, J Cogan Z, et al. Combinatorial single-cell CRISPR screens by direct guide RNA capture and targeted sequencing. Nat Biotechnol. 2020 ;38(8):954-961. PubMed
BibTex

Yan J, Cirincione A, Adamson B. Prime Editing: Precision Genome Editing by Reverse Transcription. Mol Cell. 2020 ;77(2):210-212. PubMed
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Chan MM, Smith ZD, Grosswendt S, Kretzmer H, Norman TM, Adamson B, et al. Molecular recording of mammalian embryogenesis. Nature. 2019 ;570(7759):77-82. PubMed
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Horlbeck MA, Xu A, Wang M, Bennett NK, Park CY, Bogdanoff D, et al. Mapping the Genetic Landscape of Human Cells. Cell. 2018 ;174(4):953-967.e22. PubMed
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Adamson B, Norman TM, Jost M, Cho MY, Nu?ez JK, Chen Y, et al.. A Multiplexed Single-Cell CRISPR Screening Platform Enables Systematic Dissection of the Unfolded Protein Response. Cell. 2016 ;167(7):1867-1882.e21. PubMed
BibTex

Dixit A, Parnas O, Li B, Chen J, Fulco CP, Jerby-Arnon L, et al. Perturb-Seq: Dissecting Molecular Circuits with Scalable Single-Cell RNA Profiling of Pooled Genetic Screens. Cell. 2016 ;167(7):1853-1866.e17. PubMed
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Horlbeck MA, Gilbert LA, Villalta JE, Adamson B, Pak RA, Chen Y, et al. Compact and highly active next-generation libraries for CRISPR-mediated gene repression and activation. Elife. 2016 ;5. PubMed
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Izhar L, Adamson B, Ciccia A, Lewis J, Pontano-Vaites L, Leng Y, et al. A Systematic Analysis of Factors Localized to Damaged Chromatin Reveals PARP-Dependent Recruitment of Transcription Factors. Cell Rep. 2015 ;11(9):1486-500. PubMed
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Gilbert LA, Horlbeck MA, Adamson B, Villalta JE, Chen Y, Whitehead EH, et al. Genome-Scale CRISPR-Mediated Control of Gene Repression and Activation. Cell. 2014 ;159(3):647-61. PubMed
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Sigoillot FD, Lyman S, Huckins JF, Adamson B, Chung E, Quattrochi B, et al. A bioinformatics method identifies prominent off-targeted transcripts in RNAi screens. Nat Methods. 2012 ;9(4):363-6. PubMed
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Adamson B, Smogorzewska A, Sigoillot FD, King RW, Elledge SJ. A genome-wide homologous recombination screen identifies the RNA-binding protein RBMX as a component of the DNA-damage response. Nat Cell Biol. 2012 ;14(3):318-28. PubMed
BibTex

Ciccia A, Nimonkar AV, Hu Y, Hajdu I, Achar YJagadheesh, Izhar L, et al. Polyubiquitinated PCNA recruits the ZRANB3 translocase to maintain genomic integrity after replication stress. Mol Cell. 2012 ;47(3):396-409. PubMed
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Chou DM, Adamson B, Dephoure NE, Tan X, Nottke AC, Hurov KE, et al. A chromatin localization screen reveals poly (ADP ribose)-regulated recruitment of the repressive polycomb and NuRD complexes to sites of DNA damage. Proc Natl Acad Sci U S A. 2010 ;107(43):18475-80. PubMed
BibTex

O'Connell BC, Adamson B, Lydeard JR, Sowa ME, Ciccia A, Bredemeyer AL, et al. A genome-wide camptothecin sensitivity screen identifies a mammalian MMS22L-NFKBIL2 complex required for genomic stability. Mol Cell. 2010 ;40(4):645-57. PubMed
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Britt Adamson is an Assistant Professor in the Department of Molecular Biology and the Lewis-Sigler Institute for Integrative Genomics. Dr. Adamson started her training in 2004 at the Massachusetts Institute of Technology in the laboratory of Angelika Amon. She graduated in 2005 and moved to Harvard Medical School for her graduate work. There, advised by Stephen Elledge, Dr. Adamson leveraged cutting-edge functional genomics technologies to systematically investigate mechanisms of genome integrity maintenance in human cells. She earned her PhD in 2012. Following graduate school, Dr. Adamson joined the laboratory of Jonathan Weissman at the University of California, San Francisco, where she received a postdoctoral fellowship from the Damon Runyon Cancer Research Foundation. Her postdoctoral work pioneered new approaches for functional genomics in human cells, technologies that now enable comprehensive dissection of cellular pathways and delineation of cell behaviors with unprecedented resolution. Dr. Adamson’s research interests center on how cells respond to stress, how such responses are regulated, and how they are altered in disease states.




Keystone Symposia Future of Science Fund Scholarship
Damon Runyon Cancer Research Foundation Postdoctoral Fellowship
Damon Runyon - Dale F. Frey Award for Breakthrough Scientists finalist