Ahmer, Brian

Associate Professor
Department of Microbiology

B.S., Colorado State University, 1990
Ph.D., Washington State University, 1994
Post-doc Oregon Health Sciences University 1994-1999  

Research description
Despite decades of research on E. coli and S. typhimurium, microbiologists are still unable to assign, or even convincingly predict, functions for ~30% of the open reading frames (ORFs) in the E. coli genome sequence. A further ~30% of these ORFs are predicted to encode proteins that belong to recognized families, but their specific functions remain undetermined.  It seems likely that the functions of many of these genes may not be observable using pure cultures.  In nature, such bacteria do not normally exist as pure cultures and a percentage of their genetic capacity is certainly involved with ‘mixed community’ interactions.   

Our laboratory is using an array-based approach to identify all Salmonella genes that confer a selective advantage during a coinfection.  Essentially a starting pool of transposon mutants is inoculated into normal animals or animals in which their normal flora has been perturbed or that have been infected by a second pathogen.  The bacteria are then recovered from various sites in the animal.  The DNA adjacent to the transposon insertions is then labeled and hybridized to a Salmonella genome array.  All genes that play a role in these situations are identified.  

One such system is the sdiA gene (which encodes a transcription factor of the LuxR family) which detects the N-acylhomoserine lactone (AHL) signaling molecules of other bacterial species.  Salmonella itself does not synthesize AHLs so SdiA is exclusively detecting signals emanating from other species.  SdiA is conserved in Escherichia, Salmonella, Shigella, and Klebsiella, and probably other closely related genera that have not yet been sequenced.  Interestingly, we have determined that the normal flora of numerous animals does not synthesize AHLs, and instead SdiA is detecting AHLs produced by non-resident, often pathogenic, species.  It appears that SdiA regulates genes that specifically take advantage of the battles that the host is waging with other pathogens.  We are studying at a molecular level the consequences of the sdiA-dependent detection of AHLs by Salmonella and its relatives using a mouse model in which the animal has been previously infected with Yersinia enterocolitica.  Y. enterocolitica synthesizes AHLs using the gene yenI.  Salmonella SdiA responds to the yenI-dependent AHL production of Y. enterocolitica in vitro and in mice.   

Selected Publications

Amber Lindsay and Brian M. M. Ahmer.  2005.  The effect of sdiA on biosensors of N-acylhomoserine lactones.  Journal of Bacteriology 187:  5054-5058.  

Brian M. M. Ahmer.  2004.  Cell-to-cell signaling in Escherichia coli and Salmonella enterica.  Molecular Microbiology 52:  933-945.  

Max Teplitski, Robert I. Goodier, Brian M. M. Ahmer.  2003.  Pathways leading from BarA/SirA to motility and virulence gene expression in Salmonella.  Journal of Bacteriology 185:  7257-7265.  

Jenee N. Smith and Brian M. M. Ahmer.  2003.  Detection of other microbial species by Salmonella:  Expression of the SdiA regulon.  Journal of Bacteriology 185:  1357-1366.  

Bindhu Michael, Jenee N. Smith, Simon Swift, Fred Heffron, Brian M. M. Ahmer.  2001.  SdiA of Salmonella enterica is a LuxR homolog that detects mixed microbial communities.  Journal of Bacteriology 183:  5733-5742.  

Robert I. Goodier and Brian M. M. Ahmer.  2001.  SirA orthologs affect both motility and virulence.  Journal of Bacteriology 183:  2249-2258.    

Ahmer Laboratory Personnel    

Contact  

email: ahmer.1@osu.edu
Webpage

376 Biological Sciences Building
484W. 12 Ave.
Columbus, Ohio
43210