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.








  • 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. Toxin-Antitoxin Systems as Phage Defense Elements. LeRoux, M, Laub, MT. 2022. Annu Rev Microbiol , .
    doi: 10.1146/annurev-micro-020722-013730PMID:35395167
  2. 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
  3. 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
  4. Global Analysis of the Specificities and Targets of Endoribonucleases from Escherichia coli Toxin-Antitoxin Systems. Culviner, PH, Nocedal, I, Fortune, SM, Laub, MT. 2021. mBio 12, e0201221.
    doi: 10.1128/mBio.02012-21PMID:34544284
  5. High-resolution, genome-wide mapping of positive supercoiling in chromosomes. Guo, MS, Kawamura, R, Littlehale, ML, Marko, JF, Laub, MT. 2021. Elife 10, .
    doi: 10.7554/eLife.67236PMID:34279217
  6. Activation of a signaling pathway by the physical translocation of a chromosome. Guzzo, M, Sanderlin, AG, Castro, LK, Laub, MT. 2021. Dev Cell 56, 2145-2159.e7.
    doi: 10.1016/j.devcel.2021.06.014PMID:34242584
  7. Shutoff of host transcription triggers a toxin-antitoxin system to cleave phage RNA and abort infection. Guegler, CK, Laub, MT. 2021. Mol Cell 81, 2361-2373.e9.
    doi: 10.1016/j.molcel.2021.03.027PMID:33838104
  8. Two-Component Signaling Systems Regulate Diverse Virulence-Associated Traits in Pseudomonas aeruginosa. Wang, BX, Cady, KC, Oyarce, GC, Ribbeck, K, Laub, MT. 2021. Appl Environ Microbiol 87, .
    doi: 10.1128/AEM.03089-20PMID:33771779
  9. Uncovering the basis of protein-protein interaction specificity with a combinatorially complete library. Lite, TV, Grant, RA, Nocedal, I, Littlehale, ML, Guo, MS, Laub, MT. 2020. Elife 9, .
    doi: 10.7554/eLife.60924PMID:33107822
  10. ppGpp Coordinates Nucleotide and Amino-Acid Synthesis in E. coli During Starvation. Wang, B, Grant, RA, Laub, MT. 2020. Mol Cell 80, 29-42.e10.
    doi: 10.1016/j.molcel.2020.08.005PMID:32857952
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