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Matthew K. Waldor

Researcher at Harvard University

Publications -  345
Citations -  29581

Matthew K. Waldor is an academic researcher from Harvard University. The author has contributed to research in topics: Vibrio cholerae & Virulence. The author has an hindex of 87, co-authored 322 publications receiving 26506 citations. Previous affiliations of Matthew K. Waldor include East China University of Science and Technology & Tufts University.

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Vibrio cholerae Intestinal Population Dynamics in the Suckling Mouse Model of Infection

TL;DR: The results show that for the El Tor biotype neither TCP nor OA is required for colonization of the suckling mouse large bowel, and similar percent recoveries of wild-type, TCP−, and OA− strains from the small bowel at an early time after infection suggest that TCP andOA are not required for strains of either biotype to resist bactericidal mechanisms in the sucksling mouse GI tract.
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Sequence tag–based analysis of microbial population dynamics

TL;DR: STAMP analyzes the frequency changes of genetically 'barcoded' organisms to quantify population bottlenecks and infer the founding population size and revealed infection-stage and region-specific host barriers to infection and showed unexpected V. cholerae migration counter to intestinal flow.
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LexA Cleavage Is Required for CTX Prophage Induction

TL;DR: In this paper, the authors investigated the mechanisms that regulate production of CTXφ, a temperate filamentous phage that infects Vibrio cholerae and encodes cholera toxin.
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Characterization of a higBA toxin-antitoxin locus in Vibrio cholerae.

TL;DR: Activation of endogenous HigB does not appear to be bactericidal, at least under the conditions tested, and biochemical analyses confirmed that HigA interacts with HigB.
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Genetic analysis of Vibrio parahaemolyticus intestinal colonization

TL;DR: A genome-wide screen revealed that toxR, an ancestral locus in Vibrio species, is required for V. parahaemolyticus fitness in vivo and for induction of T3SS2 gene expression, and disparate horizontally acquired virulence systems have been placed under the control of this ancestral transcription factor across independently evolved human pathogens.