Kimberley D. Seed

The paper uses anti-phage defense systems to block viral lifecycle stages and reveals that PLE activation depends on progressive transcriptional cues from the phage's developmental program.

The paper uses clinical surveillance in Bangladesh to study phage-pathogen coevolution in Vibrio cholerae, identifying a parasitic MGE that drives a selective sweep during a major outbreak.

The paper shows that restricted phage infection primes bacterial immunity to defeat counterdefenses by increasing defense protein abundance and altering host-phage stoichiometry.

This study identifies Vc OLD, a Class 1 OLD family nuclease from Vibrio cholerae, and its inhibitor Oad1 from phage ICP1, revealing their roles in phage defense and the bacterial-viral arms race.

This paper identifies how the phage-encoded inhibitor OrbA disrupts the BREX defense system in Vibrio cholerae by directly binding to the BrxC ATPase component.

The paper identifies the DarTG toxin-antitoxin system in Vibrio cholerae that inhibits the lytic phage ICP1, and shows ICP1 counters this with an antitoxin mimic, revealing co-evolutionary dynamics between the bacterium and its phage.

This study identifies Gpi, a PLE-encoded inhibitor of ICP1's DNA packaging motor, and shows how PLEs use multiple strategies to overcome inhibition and promote their own spread.

The paper shows that H-NS and TsrA regulate horizontally acquired elements in a clinical isolate of V. cholerae, with TsrA modulating H-NS activity and independently affecting gene expression.

The paper examines HEGs in bacteriophages, finding variable distribution, HEG islands, and domain swapping, suggesting HEGs significantly influence phage evolution.

The paper performs a genomic analysis of Vibrio cholerae El Tor strains from Bangladesh, identifying two lineages, BD-1 and BD-2, and their distinct genomic traits and epidemiological implications.