M. Stephen Trent

Trent , M. Stephen
Associate Professor in Molecular Genetics and Microbiology

E-mail: strent@austin.utexas.edu

Main Office: NMS 3.118
Phone: (512) 232-8371

Alternate Office: NMS 3.236
Phone: (512) 232-8372

Mailing Address:
The University of Texas at Austin
Molecular Genetics and Microbiology
2506 Speedway Stop A5000
Austin, TX 78712-1191

Graduate Students:

  • Cullen, Thomas
  • Needham, Brittany
  • Nowicki, Emily
  • Pride, Aaron

    • Post Doc Students:

  • Giles, David
  • Hankins, Jessica
  • Herrera, Carmen M

    • Research Summary:
       In order to survive, bacteria must quickly respond to changes in the surrounding environment. We are interested in how diverse environmental stimuli promote changes in conserved microbial structures found on the surface of pathogenic bacteria. Currently, our laboratory focuses on the remodeling of lipopolysaccharides or LPS. LPS, also referred to as endotoxin, is the major surface component of Gram-negative bacteria and represents one of the microbial molecular signals responsible for activation of the host innate immune system. Our goal is to identify and characterize the molecular mechanisms necessary for the remodeling of LPS, and to determine how alteration of LPS contributes to evasion of the innate immune response during infection. Several pathogenic bacteria are under investigation in our laboratory including Vibrio cholerae, Campylobacter jejuni, Helicobacter pylori, Salmonella typhimurium, and pathogenic strains of Escherichia coli. Understanding how bacteria remodel their cell surface is of fundamental importance and may yield new therapeutic strategies for intervention in bacterial infections.
     
    Publications:
    Virulence and stress-related periplasmic protein (VisP) in bacterial/host 2 associations (2012) PNAS, In press.
    The polysaccharide capsule of Campylobacter jejuni 81-176 modulates the host immune response (2012) Infection and Immunity, In press.
    The Pseudomonas aeruginosa PhoP-PhoQ two-component regulatory system is induced upon interaction with epithelial cells and controls cytotoxicity and inflammation (2012) Infection and Immunity 80, 3122-31.
    Modulating the Innate Immune Response by Combinatorial Engineering of Endotoxin (2012) PNAS, In press.
    EptC of Campylobacter jejuni mediates phenotypes involved in host interactions and virulence (2012) Infection and Immunity, In press.
    Amino acid addition to Vibrio cholera LPS establishes a link between surface remodeling in Gram-negative and Gram-positive bacteria. (2012) PNAS 109, 8722-7.
    Characterization of a unique modification of the flagellar rod protein FlgG by the Campylobacter jejuni lipid A phosphoethanolamine transferase, linking bacterial locomotion and antimicrobial peptide resistance (2012) J. Bio. Chem. 287, 3326-36.
    Helicobacter pylori Versus The Host: Remodeling Of The Bacterial Outer Membrane Is Required For Survival In The Gastric Mucosa (2011) PLoS Pathogens 7, 1-18.
    Elucidation of a novel Vibrio cholerae lipid A secondary hydroxy-acyltransferase and its role in innate immune recognition (2011) Mol Microbiol 81, 1313-29.
    IR and UV Photodissociation as Analytical Tools for Charaacterizing Lipid A Structures (2011) Anal Chem 83, 5107-13.
    The pmrCAB operon mediates polymyxin resistance in Acinetobacter baumannii ATCC 17878 and clinical isolates through phosphoethanolamine modification of lipid A (2011) Antimicrob Agents Chemother 55, 3743-51.
    Remodeling of Vibrio cholerae membranes by incorporation of exogenous fatty acids from host and acquatic environments (2011) Mol Microbiol 79, 716-28.
    Removal of the outer Kdo from Heliobacter pylori lipopolysaccharide and its impact on the bacterial surface (2010) Mol Microbiol 78, 837-52.
    Activation of PmrA inhibits LpxT-dependent phosphorylation of lipid A promoting resistance to antimicrobial peptides (2010) Mol Microbiol 76, 1444-60.
    A link between the assembly of flagella and lipooligosaccharide of the Gram-negative bacterium Campylobacter jejuni (2010) PNAS. 107, 5160-5.
    Active site architecture and catalytic mechanism of the lipid A deacylase LpxR of Salmonella typhimurium (2009) PNAS. 106, 1960-4.
    Phosphorylation of Kdo is required for secondary acylation of the V. cholerae lipopolysaccharide (2009) J. Bio. Chem. 284, 25804-12.
    Synthesis of and Evaluation of Lipid A Modification by 4-Substituted 4-Deoxy Arabinose Anaolgs as Potential Inhibitors of Bacterial Polymyxin Resistance (2008) Biorg. & Med. Chem. Letters 18, 1507-10.
    Periplasmic phosphorylation of lipid A is linked to the synthesis of undecaprenyl phosphate (2008) Mol. Micro. 67, 264-277.
    The LptA protein of Escherichia coli is a periplasmic lipid A binding protein involved in the lipopolysaccharide export pathway (2008) J. Biol. Chem. 283, 20342-9.
    Deciphering the unusual acylation pattern of Helicobacter pylori lipid A (2008) J. Bacteriology 190, 7012-21.
    Lipid A modification systems of Gram-negative bacteria (2007) Annual Rev. of Biochem. 76, 295-329.
    The Pseudomonas aeruginosa Deacylase (PagL) required for synthesis of cystic fibrosis-specific lipid A (2006) J. Bacteriology 188, 191-201.
    Diversity of Endotoxin and its Impact on Pathogenesis (2006) J. of Endotoxin Res. 12, 205-223.
    The Lipid A 1-Phosphatase of Helicobacter pylori is Required for Antimicrobial Peptide Resistance (2006) J. Bacteriology 188, 4531-4541.
    Diversity of Endotoxin and its Impact on Pathogenesis (2006) J. of Endotoxin Res. 12, 205-223.
    The Lipid A 1-Phosphatase of Helicobacter pylori is Required for Antimicrobial Peptide Resistance (2006) J. Bacteriology 188, 4531-4541.
    An outer membrane enzyme in Salmonella typhimurium that removes the 3ยด-acyloxyacyl moiety of lipid A (2006) J. Biol. Chem. 281, 21974-87.
    Remodeling of Helicobacter pylori lipopolysaccharides (2005) J. of Endotoxin Res. 11, 161-6.
    Resistance to the antimicrobial peptide polymyxin requires secondary myristoylation of Gram-negative bacterial lipid A (2005) J. Biol. Chem. 280, 28186-94.
    A Novel Kdo-Hydrolase that removes the outer Kdo sugar from Helicobacter pylori lipopolysaccharide (2005) J. Bacteriology 187, 3374-83.
    Biosynthesis, Transport, and Modification of Lipid A (2004) Biochemistry and Cell Biology 82, 71-86.
    Periplasmic Cleavage and Modification of the 1-Phosphate Group of Helicobacter pylori Lipid A (2004) J. Biol. Chem. 279, 55780-91.

     
    Search PubMed for more publications by Prof. Name
    (a new browser window will open)
    "Caution, this search may require more information to be accurate or specific. Check authors and institution carefully."

    Max Docs:  Pub. Date limit: