Bacterial stress response, metabolic shut-down, signal transduction, gene regulatory networks

Background and Training

PhD: Dartmouth College

Postdoctoral training: Mount Holyoke College

Research Summary

Diverse bacterial species live all around us. Even with their seemingly simplistic genomes and cell structure, bacteria can adapt to an enormous range of environments and are often equipped to survive in extremely inhospitable places.  This is generally advantageous for the microorganism, but can have variable impacts on other species, including humans.

My research focuses on aspects of bacterial stress response. When faced with nutrient depletion or stress, some bacterial species transition from actively growing cells to dormant cells known as spores.  During sporulation, a bacterial cell divides asymmetrically resulting in two cells of different sizes that lie side-by-side.  The larger cell (mother cell) supports the development of the smaller cell (forespore), but ultimately dies. The forespore goes on to become a mature spore.  Mature spores are extremely resistant to environmental stressors and are believed to be able to survive for thousands of years in this dormant state. For this reason, spores are hard to eradicate and are often associated with difficult to treat infections, such as those caused by the pathogen Clostridium difficile.

Bacillus subtilis has been studied for decades as a model organism for spore formation, yet the mechanism by which essential metabolic functions in the developing forespore are powered has not been fully elucidated. One model is that the mother cell “feeds” the forespore through a channel apparatus, which forms between the mother cell and the forespore during development (Camp et al. 2009, Doan et al. 2009). My work focuses on understanding how the metabolic shift in the forespore is coordinated, and how it is influenced by the channel. I use a variety of genetic, transcriptomic, and biochemical analyses to map out specific changes in the forespore metabolic profile during sporulation.  I also use the sporulation genetic program as a model to understand how bacteria fine-tune genetic regulation at transcriptional and translational levels.


  • Mearls, E.B., J Jackter, J. Colquhoun, V. Farmer, A. Matthews, L. Murphy, C. Fenton, and A.H. Camp. Transcription and translation of the sigG gene is tuned for proper execution of the switch from early to late gene expression in the developing Bacillus subtilis spore. PLoS Genet. 2018 Apr; 14(4): e1007350.
  • Flanagan K.A., J. Comber, E.B. Mearls, C. Fenton, A.F. Wang Erickson, R. Losick, and A.H. Camp: A Membrane-Embedded Amino Acid Couples the SpoIIQ Channel Protein to Anti-Sigma Factor Transcriptional Repression during Bacillus subtilis Sporulation. J. Bacteriol. 2016 Apr;14;198(9):1451-63
  • Mearls E.B., D.R. Olson, C.D. Herring, and L.R. Lynd: Development of a regulatable plasmid based gene expression system for Clostridium thermocellum. Appl. Microbiol. Biotechnol. 2015 Sep; 18:7589-99
  • Mearls E.B., L.R. Lynd.: The identification of four histidine kinases that influence sporulation in Clostridium thermocellum. Anaerobe. 2014 Jun; 28:109-119
  • Mearls E.B., J.A. Izquierdo, L.R. Lynd: Formation and characterization of non-growth states in Clostridium thermocellum: spores and L-forms. BMC Microbiology 2012 Jun; 12:180.