Ellen Rothenberg is a molecular immunologist known for her work on gene regulation and development of T lymphocytes and how transcription factor gene networks drive the emergence of T-cell identity. Born in Massachusetts in an academic family, she grew up mostly in the Chicago and Boston areas. She received her bachelor’s degree in Biochemical Sciences from Harvard University and her Ph.D. on retroviral DNA replication from the Massachusetts Institute of Technology. She moved to study T-cell development with a Jane Coffin Childs Postdoctoral Fellowship at Memorial Sloan-Kettering Cancer Center and an Assistant Research Professorship at The Salk Institute. She came to the California Institute of Technology (Caltech) in 1982 and rose to become Albert Billings Ruddock Professor in 2007, then Distinguished Professor in 2021. She has been elected Fellow of the American Association for the Advancement of Science, Fellow of the American Academy of Arts and Sciences, and Member of the National Academy of Sciences. She was also selected for the inaugural class of Distinguished Fellows of the American Association of Immunologists. She won the Richard P. Feynman Prize for Excellence in Teaching and eight other teaching awards at Caltech, and has taught internationally on immunology, developmental biology, and gene regulatory networks.

Research Interests

Ellen Rothenberg's research focuses on gene networks controlling hematopoietic cell fates, the interplay between transcription factors and chromatin, and mechanisms underlying the dynamics of single-cell developmental decisions. Her group studies how multipotent hematopoietic precursors, after entering the thymus, exclude other developmental options and undergo commitment to a T-cell fate. First, the group tracked how this lineage choice becomes cell-intrinsic, combining high-resolution flow cytometry, alternative in vitro differentiation conditions, and transcriptome analyses, and identified cohorts of transcription factors dynamically regulated during commitment. Using stage-specific gain and loss of function perturbations for gene network analyses, key transcription factors were identified with commitment-delaying, commitment-enhancing, commitment-reversing, or lineage-choice redirecting functions, notably PU.1, which supports multipotency, and Bcl11b, which promotes commitment. The group?s recent focus has been on causality. Live imaging of normal or perturbed differentiation revealed how the distinctive kinetics of commitment emerge at the single-cell level, showing that protein stability and mitotic dilution strongly affect the gene network effects of PU.1, and that slow chromatin remodeling strongly retards Bcl11b activation timing. Genome-wide analyses showed that while transcription factor binding choices can be constrained by inherited chromatin states, factors like PU.1 and Bcl11b interact with other factors, redeploying them to alternative genomic sites. These effects emerge as developmental channeling and irreversibility.

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Primary Section

Section 43: Immunology and Inflammation

Secondary Section

Section 22: Cellular and Developmental Biology