Michael T. Laub

Michael T. Laub

Professor of Biology; Associate Department Head; Director of Scientific Operations, Building 68; 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.

617-324-0418

Phone

68-580

Office

laub@mit.edu

Email

Tau Zaman

Assistant

617-452-2717

Assistant Phone

Education

PhD 2002, Stanford University

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.

Awards

  • 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. Global Analysis of the E. coli Toxin MazF Reveals Widespread Cleavage of mRNA and the Inhibition of rRNA Maturation and Ribosome Biogenesis. Culviner, PH, Laub, MT. 2018. Mol. Cell 70, 868-880.e10.
    doi: 10.1016/j.molcel.2018.04.026PMID:29861158
  2. Global analysis of double-strand break processing reveals in vivo properties of the helicase-nuclease complex AddAB. Badrinarayanan, A, Le, TBK, Spille, JH, Cisse, II, Laub, MT. 2017. PLoS Genet. 13, e1006783.
    doi: 10.1371/journal.pgen.1006783PMID:28489851
  3. Contact-dependent killing by Caulobacter crescentus via cell surface-associated, glycine zipper proteins. García-Bayona, L, Guo, MS, Laub, MT. 2017. Elife 6, .
    doi: 10.7554/eLife.24869PMID:28323618
  4. The small membrane protein MgrB regulates PhoQ bifunctionality to control PhoP target gene expression dynamics. Salazar, ME, Podgornaia, AI, Laub, MT. 2016. Mol. Microbiol. 102, 430-445.
    doi: 10.1111/mmi.13471PMID:27447896
  5. Transcription rate and transcript length drive formation of chromosomal interaction domain boundaries. Le, TB, Laub, MT. 2016. EMBO J. 35, 1582-95.
    doi: 10.15252/embj.201593561PMID:27288403
  6. The bacterial cell cycle regulator GcrA is a σ70 cofactor that drives gene expression from a subset of methylated promoters. Haakonsen, DL, Yuan, AH, Laub, MT. 2015. Genes Dev. 29, 2272-86.
    doi: 10.1101/gad.270660.115PMID:26545812
  7. Identification of the PhoB Regulon and Role of PhoU in the Phosphate Starvation Response of Caulobacter crescentus. Lubin, EA, Henry, JT, Fiebig, A, Crosson, S, Laub, MT. 2016. J. Bacteriol. 198, 187-200.
    doi: 10.1128/JB.00658-15PMID:26483520
  8. Evolving new protein-protein interaction specificity through promiscuous intermediates. Aakre, CD, Herrou, J, Phung, TN, Perchuk, BS, Crosson, S, Laub, MT. 2015. Cell 163, 594-606.
    doi: 10.1016/j.cell.2015.09.055PMID:26478181
  9. Rapid pairing and resegregation of distant homologous loci enables double-strand break repair in bacteria. Badrinarayanan, A, Le, TB, Laub, MT. 2015. J. Cell Biol. 210, 385-400.
    doi: 10.1083/jcb.201505019PMID:26240183
  10. Protein evolution. Pervasive degeneracy and epistasis in a protein-protein interface. Podgornaia, AI, Laub, MT. 2015. Science 347, 673-7.
    doi: 10.1126/science.1257360PMID:25657251
More Publications