Since 2023
Tran, M., Hernandez Viera, A. J., Rosu, J., Tran, P. Q., Goldman, D. A., and Mo, C. Y. (2026). Staphylococcus epidermidis Genomic Plasticity Modulates Horizontal Gene Transfer.
Hofman, R., Herman, C., Mo, C. Y., Mathai, J., and Marraffini, L. A. (2025) Deep mutational scanning identifies Cas1 and Cas2 variants that enhance type II-A CRISPR-Cas spacer acquisition. Nature Communications 16, 5730. https://doi.org/10.1038/s41467-025-60925-9
Chen, J., Nilsen, E. D., Chitboonthavisuk, C., Mo, C. Y., and Raman, S. (2025). Systematic, high-throughput characterization of bacteriophage gene essentiality on diverse hosts. Cell Host & Microbe. (in press); Preprint: https://www.biorxiv.org/content/10.1101/2024.10.10.617714v1
Tran, M.,* Hernandez Viera, A. J.,* Tran, P. Q., Nilsen, E.D., Tran, L., and Mo, C. Y. (2025). Bacteriophage infection drives loss of β-lactam resistance in methicillin-resistant Staphylococcus aureus. eLife 13:RP102743. https://doi.org/10.7554/eLife.102743.3 *denotes equal contribution.
Mo, C.Y. (2024). If you can’t beat them, join them: Anti-CRISPR proteins derived from CRISPR-associated genes. Cell Host & Microbe. 2(11): 1871-1873.
Before 2023
Mo, C.Y., Mathai, J., Rostøl, J.T., Varble, A., Banh, D.V., and Marraffini, L.A. (2021). Type III-A CRISPR immunity promotes mutagenesis of staphylococci. Nature 592, 611–615. 10.1038/s41586-021-03440-3.
Jia, N., Mo, C.Y., Wang, C., Eng, E.T., Marraffini, L.A., and Patel, D.J. (2019). Type III-A CRISPR-Cas Csm Complexes: Assembly, Periodic RNA Cleavage, DNase Activity Regulation, and Autoimmunity. Molecular Cell 73, 264-277.e5. 10.1016/j.molcel.2018.11.007.
Wang, L., Mo, C.Y., Wasserman, M.R., Rostøl, J.T., Marraffini, L.A., and Liu, S. (2019). Dynamics of Cas10 Govern Discrimination between Self and Non-self in Type III CRISPR-Cas Immunity. Molecular Cell 73, 278-290.e4. 10.1016/j.molcel.2018.11.008.
Mo, C.Y., and Marraffini, L.A. (2018). If You’d Like to Stop a Type III CRISPR Ribonuclease, Then You Should Put a Ring (Nuclease) on It. Molecular Cell 72, 608–609. 10.1016/j.molcel.2018.10.048.
Culyba, M.J., Kubiak, J.M., Mo, C.Y., Goulian, M., and Kohli, R.M. (2018). Non-equilibrium repressor binding kinetics link DNA damage dose to transcriptional timing within the SOS gene network. PLoS Genet 14, e1007405. 10.1371/journal.pgen.1007405.
Selwood, T., Larsen, B.J., Mo, C.Y., Culyba, M.J., Hostetler, Z.M., Kohli, R.M., Reitz, A.B., and Baugh, S.D.P. (2018). Advancement of the 5-Amino-1-(Carbamoylmethyl)-1H-1,2,3-Triazole-4-Carboxamide Scaffold to Disarm the Bacterial SOS Response. Front. Microbiol. 9, 2961. 10.3389/fmicb.2018.02961.
Mo, C.Y., Culyba, M.J., Selwood, T., Kubiak, J.M., Hostetler, Z.M., Jurewicz, A.J., Keller, P.M., Pope, A.J., Quinn, A., Schneck, J., et al. (2018). Inhibitors of LexA Autoproteolysis and the Bacterial SOS Response Discovered by an Academic–Industry Partnership. ACS Infect. Dis. 4, 349–359. 10.1021/acsinfecdis.7b00122.
Kubiak, J.M., Culyba, M.J., Liu, M.Y., Mo, C.Y., Goulian, M., and Kohli, R.M. (2017). A Small-Molecule Inducible Synthetic Circuit for Control of the SOS Gene Network without DNA Damage. ACS Synth. Biol. 6, 2067–2076. 10.1021/acssynbio.7b00108.
Mo, C.Y., Manning, S.A., Roggiani, M., Culyba, M.J., Samuels, A.N., Sniegowski, P.D., Goulian, M., and Kohli, R.M. (2016). Systematically Altering Bacterial SOS Activity under Stress Reveals Therapeutic Strategies for Potentiating Antibiotics. mSphere 1, e00163-16. 10.1128/mSphere.00163-16.
Culyba, M.J., Mo, C.Y., and Kohli, R.M. (2015). Targets for Combating the Evolution of Acquired Antibiotic Resistance. Biochemistry 54, 3573–3582. 10.1021/acs.biochem.5b00109.
Gajula, K.S., Huwe, P.J., Mo, C.Y., Crawford, D.J., Stivers, J.T., Radhakrishnan, R., and Kohli, R.M. (2014). High-throughput mutagenesis reveals functional determinants for DNA targeting by activation-induced deaminase. Nucleic Acids Research 42, 9964–9975. 10.1093/nar/gku689.
Mo, C.Y., Birdwell, L.D., and Kohli, R.M. (2014). Specificity Determinants for Autoproteolysis of LexA, a Key Regulator of Bacterial SOS Mutagenesis. Biochemistry 53, 3158–3168. 10.1021/bi500026e.