Caleb Mallery

Caleb Mallery, a fourth-year PhD candidate in the Paczkowski Lab within the Division of Genetics at the Wadsworth Center and a student in the Department of Biomedical Sciences at the University at Albany, has been awarded a prestigious F31 predoctoral fellowship from the National Institute of Allergy and Infectious Diseases at the National Institutes of Health. His research focuses on Pseudomonas aeruginosa, a significant cause of hospital-acquired infections, particularly among individuals with cystic fibrosis and those with weakened immune systems. This pathogen relies on quorum sensing – a process by which bacteria coordinate gene expression based on population density – to regulate virulence, including biofilm formation and toxin production.

His work centers on RhlR, a key transcription factor that activates virulence genes in response to quorum sensing signals, and its interaction with the protein PqsE. Mallery’s recent findings demonstrate that in the absence of PqsE, the Lon protease rapidly degrades RhlR, effectively shutting down quorum sensing.

Through this fellowship, Mallery will investigate the molecular mechanisms underlying this process. He hypothesizes that RhlR contains a degradation signal that is masked by PqsE under normal conditions but becomes exposed when PqsE levels decrease, triggering targeted degradation. His research aims to define this signal and determine how it regulates the timing of virulence in response to bacterial population density.

The three-year, $115,878 NIH Ruth L. Kirschstein National Research Service Award F31 was awarded following review by a panel of experts in microbiology and infectious disease, who recognized Mallery as an outstanding candidate with strong scholarly productivity, including a first-author publication in mBio and co-authored work in Nature Communications and the Journal of Bacteriology.

This fellowship will support the final years of his doctoral training and his development toward a career as an independent investigator in infectious disease research.

Read more:

Evolution of PqsE as a Pseudomonas aeruginosa-specific regulator of LuxR-type receptors: insights from Pseudomonas and Burkholderia

Expanding the LuxR-type receptor functional repertoire: Protein-protein interactions in quorum sensing regulation

RhlR quorum-sensing receptor ligand sensitivity regulates the differential expression of phenazine genes in Pseudomonas aeruginosa

Quorum-sensing synthase mutations re-calibrate autoinducer concentrations in clinical isolates of Pseudomonas aeruginosa to enhance pathogenesis

More News