Michael T. Laub

Michael T. Laub

Professor of Biology; Co-Chair, Biology Diversity, Equity, and Inclusion (DEI) Faculty Committee; Member, DEI Council; Investigator, Howard Hughes Medical Institute

Michael T. Laub explores how bacterial cells process information and regulate their own growth and proliferation, as well as how these information-processing capabilities have evolved.







Building 68 - Koch Biology Building


Martha Pham



Assistant Phone


  • PhD, 2002, Stanford University
  • BS, 1997, Molecular Biology, University of California, San Diego

Research Summary

We study the biological mechanisms and evolution of how cells process information to regulate their own growth and proliferation. Using bacteria as a model organism, we aim to elucidate the detailed molecular basis for this remarkable regulatory capability, and understand the selective pressures and mechanisms that drive the evolution of signaling pathways. Our work is rooted in a desire to develop a deeper, fundamental understanding of how cells function and evolve, but it also has important medical implications since many signaling pathways in pathogenic bacteria are needed for virulence.


  • Howard Hughes Medical Institute, HHMI Investigator, 2015
  • National Science Foundation, Presidential Early Career Award for Scientists and Engineers, 2010
  • Howard Hughes Medical Institute, Early Career Scientist, 2009

Recent Publications

  1. Marginal specificity in protein interactions constrains evolution of a paralogous family. Ghose, DA, Przydzial, KE, Mahoney, EM, Keating, AE, Laub, MT. 2023. Proc Natl Acad Sci U S A 120, e2221163120.
    doi: 10.1073/pnas.2221163120PMID:37098061
  2. Direct activation of a bacterial innate immune system by a viral capsid protein. Zhang, T, Tamman, H, Coppieters 't Wallant, K, Kurata, T, LeRoux, M, Srikant, S, Brodiazhenko, T, Cepauskas, A, Talavera, A, Martens, C et al.. 2022. Nature 612, 132-140.
    doi: 10.1038/s41586-022-05444-zPMID:36385533
  3. Prophage-like gene transfer agents promote Caulobacter crescentus survival and DNA repair during stationary phase. Gozzi, K, Tran, NT, Modell, JW, Le, TBK, Laub, MT. 2022. PLoS Biol 20, e3001790.
    doi: 10.1371/journal.pbio.3001790PMID:36327213
  4. A functional selection reveals previously undetected anti-phage defence systems in the E. coli pangenome. Vassallo, CN, Doering, CR, Littlehale, ML, Teodoro, GIC, Laub, MT. 2022. Nat Microbiol 7, 1568-1579.
    doi: 10.1038/s41564-022-01219-4PMID:36123438
  5. The evolution of a counter-defense mechanism in a virus constrains its host range. Srikant, S, Guegler, CK, Laub, MT. 2022. Elife 11, .
    doi: 10.7554/eLife.79549PMID:35924892
  6. The DarTG toxin-antitoxin system provides phage defence by ADP-ribosylating viral DNA. LeRoux, M, Srikant, S, Teodoro, GIC, Zhang, T, Littlehale, ML, Doron, S, Badiee, M, Leung, AKL, Sorek, R, Laub, MT et al.. 2022. Nat Microbiol 7, 1028-1040.
    doi: 10.1038/s41564-022-01153-5PMID:35725776
  7. Ancestral reconstruction of duplicated signaling proteins reveals the evolution of signaling specificity. Nocedal, I, Laub, MT. 2022. Elife 11, .
    doi: 10.7554/eLife.77346PMID:35686729
  8. Toxin-Antitoxin Systems as Phage Defense Elements. LeRoux, M, Laub, MT. 2022. Annu Rev Microbiol 76, 21-43.
    doi: 10.1146/annurev-micro-020722-013730PMID:35395167
  9. Co-evolution of interacting proteins through non-contacting and non-specific mutations. Ding, D, Green, AG, Wang, B, Lite, TV, Weinstein, EN, Marks, DS, Laub, MT. 2022. Nat Ecol Evol 6, 590-603.
    doi: 10.1038/s41559-022-01688-0PMID:35361892
  10. Escherichia coli SymE is a DNA-binding protein that can condense the nucleoid. Thompson, MK, Nocedal, I, Culviner, PH, Zhang, T, Gozzi, KR, Laub, MT. 2022. Mol Microbiol 117, 851-870.
    doi: 10.1111/mmi.14877PMID:34964191
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