Janelle Hare

I am a microbiologist enjoys conducting research with students on the regulatory responses of bacteria to environmental stimuli, and the regulation & evolution of bacterial pathogenicity. My model organism is Acinetobacter baumannii, an opportunistic pathogen that the CDC has deemed an urgent threat because of its high levels of antibiotic resistance. Our goal is to learn how this pathogen responds to the to stressors such as DNA damage induced by UV light exposure or the presence of antibiotics such as are commonly found in hospital settings. Typically, bacteria experiencing DNA damage will halt their growth while they fix the damage, but the same response can also induce error-prone polymerases to replicate the damaged DNA, causing mutations. My lab members use microbiological, molecular biological, biochemical, next-generation sequencing, and bioinformatics techniques to decipher and compare the responses to DNA damage to learn how this process is regulated and what genes are important to Acinetobacter under these situations.  

• Cook, D., M. Flannigan, B. Candra, K. Compton, and J. M. Hare. 2022. The DdrR coregulator of the Acinetobacter baumannii mutagenic DNA damage response potentiates UmuDAb repression of error-prone polymerases. Journal of Bacteriology 204(11): 1-15. doi/10.1128/jb.00165-22. 
• Cook, D., J. Carrington, K. Johnson, and J. M. Hare. 2021. Homodimerization and Heterodimerization Requirements of Acinetobacter baumannii SOS Response Coregulators UmuDAb and DdrR revealed by Two-Hybrid Analyses. Canadian Journal of Microbiology. 67:358-371. doi.org/10.1139/cjm-2020-0219. 
• Peterson, M. A., A. N. Grice, and J. M. Hare. 2020. A corepressor participates in LexA-independent regulation of error-prone polymerases in Acinetobacter. Microbiology. 166(2): 212-226. doi.org/10.1099/mic.0.000866. 
• Witkowski, T.*, A. N. Grice, M. A. Peterson*, D. B. Stinnett*, W. K. Wells*, and J. M. Hare. 2016. UmuDAb: An error-prone polymerase accessory homolog whose N-terminal domain is required for repression of DNA damage inducible gene expression in Acinetobacter baylyi. PLOS ONE 10.1371/journal.pone.0152013.  
• Hare, J.M., J.* Ferrell, T.* Witkowski, A. N. Grice. 2014. Prophage induction and differential RecA and UmuDAb transcriptome regulation in the DNA damage responses of Acinetobacter baumannii and Acinetobacter baylyi. PLOS ONE 9(4): e93861. doi:10.1371/journal.pone.0093861.  
• J.M. Hare, J. A. Bradley*, T. J. Elam*, and Ching-li Lin*. 2012. Diverse DNA damage responses in Acinetobacter include the capacity for DNA damage-induced mutagenesis in the opportunistic pathogens Acinetobacter baumanniiand Acinetobacter ursingii. Microbiology 158: 601-611. doi.org/10.1099/mic.0.054668-0 
• J.M. Hare, S. Adhikari*, K. V. Lambert*, A. E. Hare and A. N Grice. 2012. The Acinetobacter Regulatory UmuDAb Protein Cleaves in Response to DNA Damage with Chimeric LexA/UmuD Characteristics. FEMS Microbiology Letters 334: 57-65. doi.org/10.1111/j.1574-6968.2012.02618.x. 
• J. M. Hare, S. N. Perkins, and L. A. Gregg-Jolly. 2006. A constitutively expressed, truncated umuDC regulates the recA-dependent DNA damage-induction of a gene in Acinetobacter baylyi strain ADP1. Applied and Environmental Microbiology 72:4036-4043. doi.org/10.1128/AEM.02774-05