Richard Johnson, PhD

Education
- B.S. Biology James Madison University
- Ph.D. Biomedical Sciences SUNY Albany School of Public Health-Wadsworth Center
- Postdoc Dept. Microbiology and Immunology, UNC at Chapel Hill
Research
I am interested in understanding how bacteria sense and adapt to their environment. My doctoral work focused on studying how intracellular Mycobacterium tuberculosis uses the universal second messenger cyclic-AMP to adapt its physiology to intracellular survival while also exporting cyclic-AMP to disrupt the antimicrobial functions of macrophages. As a postdoc, I examined how pathogenic Bordetella species, including the causative agents of pertussis (aka ‘whooping cough’) and kennel cough, deliver their virulence factors to mammalian cells.
Our lab uses Bordetella bronchiseptica to study interactions between bacteria and the host immune system in the context of natural host infection. We have projects examining how Bordetella uses a two-partner secretion system to sense and respond to contact with host cells, characterizing novel antimicrobials that disrupt vital secretion machinery, and leveraging bacterial heterogeneity to identify novel virulence factors essential for Bordetella pathogenesis.
Patents
- International patent PCT/AU2025/050953 Filed 29-08-2025
- Title of Invention: Two-partner secretion system binding compounds
- Inventors: Matthew Thomas Doyle, Alfred Hartojo, Peggy Cotter, Richard Johnson
Publications
- Wolber AR, McKay LS, Mote KB, Johnson R.M., Inatsuka CS, Cotter PA. Nuanced differences in adenylate cyclase toxin production, acylation, and secretion may contribute to the evolution of virulence in Bordetella species. mBio. 2025 May 19.
- Nash ZM, Inatsuka CS, Cotter PA, Johnson R.M*., 2024. Bordetella filamentous hemagglutinin and adenylate cyclase toxin interactions on the bacterial surface are consistent with FhaB-mediated delivery of ACT to phagocytic cells. mBio 15:e00632-24.
- McKay LS, Spandrio AR, Johnson R.M., Sobran MA, Marlatt SA, et al. (2024) Cytochrome oxidase requirements in Bordetella reveal insights into evolution towards life in the mammalian respiratory tract. PLoS Pathogens 20(7): e1012084.
- McDowell J.R., Bai, G., Lasek-Nesselquist E., Eisele, L.E., Wu, Y., Hurteau, G., Johnson R.M., Bai Y., Chen, Y., Chan, J., McDonough, K.A. Mycobacterial phosphodiesterase Rv0805 is a virulence determinant and its cyclic nucleotide hydrolytic activity is required for propionate detoxification. Mol. Microbiol.119, 401-422 (2023).
- Barr S.A., Kennedy E.N., McKay L.S, Johnson, R.M., Ohr, R.J., Cotter, P.A., Bourret R.B. Phosphorylation chemistry of the Bordetella PlrSR TCS and its contribution to bacterial persistence in the lower respiratory tract. Mol. Microbiol. 119, 174–19 (2023).
- Johnson R.M., Nash ZM, Dedloff MR, Shook JC, Cotter PA. DegP Initiates Regulated Processing of Filamentous Hemagglutinin in Bordetella bronchiseptica. mBio. 2021 Jun 29:e0146521.
- Johnson, R.M. and McDonough, K.A. Nucleotide signaling in Mycobacteria: an expanding repertoire. FEMS Pathog Disease, 2018 Jul; 76(5).
- Johnson R.M., Bai, G., DeMott, C.M., Banavali, N.K., Montague, C.R., Moon, C., Shekhtman, A., VanderVen, B., McDonough, K.A. Chemical Activation of adenylyl cyclase Rv1625c inhibits growth of Mycobacterium tuberculosis on cholesterol and modulates intramacrophage signaling. Mol. Microbiol. 2017 Jul;105(2):294-308.
- Complete record of publications – https://orcid.org/0000-0002-0355-889X