Rebecca Lamason

Rebecca Lamason

Associate Professor of Biology

Rebecca Lamason investigates what happens when cellular functions are hijacked by unwanted interlopers: namely, the bacteria that engender diseases like spotted fever and meningitis.

617-258-6155

Phone

68-670A

Office

rlamason@mit.edu

Email

Building 68 - Koch Biology Building

Location

Lab Website
Tori Yetman

Assistant

617-258-6473

Assistant Phone

Education

  • PhD, 2011, The Johns Hopkins University School of Medicine
  • BS, 2002, Molecular Biology and Biotechnology, Millersville University

Research Summary

In the Lamason lab, we investigate how intracellular bacterial pathogens hijack host cell processes to promote infection. In particular, we study how Rickettsia parkeri and Listeria monocytogenes move through our tissues via a process called cell-to-cell spread. We utilize cellular, molecular, genetic, biochemical and biophysical approaches to elucidate the mechanisms of spread in order to reveal key aspects of pathogenesis and host cell biology.

Awards

  • NIH Pathway to Independence Award, 2015

Recent Publications

  1. Pathogen-induced rerouting of host membrane trafficking. Woida, PJ, Lamason, RL. 2025. Curr Opin Cell Biol 94, 102520.
    doi: 10.1016/j.ceb.2025.102520PMID:40262416
  2. Rickettsia parkeri forms extensive, stable contacts with the rough endoplasmic reticulum. Acevedo-Sánchez, Y, Woida, PJ, Anderson, C, Kraemer, S, Lamason, RL. 2025. J Cell Biol 224, .
    doi: 10.1083/jcb.202406122PMID:39775737
  3. A conserved interaction between the effector Sca4 and host clathrin suggests additional contributions for Sca4 during rickettsial infection. Vondrak, CJ, Sit, B, Suwanbongkot, C, Macaluso, KR, Lamason, RL. 2024. Infect Immun 92, e0026724.
    doi: 10.1128/iai.00267-24PMID:39535192
  4. Cell-selective proteomics reveal novel effectors secreted by an obligate intracellular bacterial pathogen. Sanderlin, AG, Kurka Margolis, H, Meyer, AF, Lamason, RL. 2024. Nat Commun 15, 6073.
    doi: 10.1038/s41467-024-50493-9PMID:39025857
  5. A conserved interaction between the effector Sca4 and host endocytic machinery suggests additional roles for Sca4 during rickettsial infection. Vondrak, CJ, Sit, B, Suwanbongkot, C, Macaluso, KR, Lamason, RL. 2024. bioRxiv , .
    doi: 10.1101/2024.06.24.600492PMID:38979345
  6. An expanded genetic toolkit for inducible expression and targeted gene silencing in Rickettsia parkeri. McGinn, J, Wen, A, Edwards, DL, Brinkley, DM, Lamason, RL. 2024. J Bacteriol 206, e0009124.
    doi: 10.1128/jb.00091-24PMID:38842342
  7. An expanded genetic toolkit for inducible expression and targeted gene silencing in Rickettsia parkeri. McGinn, J, Wen, A, Edwards, DL, Brinkley, DM, Lamason, RL. 2024. bioRxiv , .
    doi: 10.1101/2024.03.15.585227PMID:38559073
  8. Pathogenic Rickettsia spp. as emerging models for bacterial biology. Sit, B, Lamason, RL. 2024. J Bacteriol 206, e0040423.
    doi: 10.1128/jb.00404-23PMID:38315013
  9. Cell-selective proteomics reveal novel effectors secreted by an obligate intracellular bacterial pathogen. Sanderlin, AG, Margolis, HK, Meyer, AF, Lamason, RL. 2023. bioRxiv , .
    doi: 10.1101/2023.11.17.567466PMID:38014272
  10. An obligate intracellular bacterial pathogen forms a direct, interkingdom membrane contact site. Acevedo-Sánchez, Y, Woida, PJ, Kraemer, S, Lamason, RL. 2023. bioRxiv , .
    doi: 10.1101/2023.06.05.543771PMID:37333133
More Publications

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