Robert Clubb
University of California-Los Angeles, CA·Biochemistry
Disease-causing bacteria such as Corynebacterium diphtheriae, the cause of diphtheria, and Staphylococcus aureus have a thick outer cell wall. They load this wall with molecules that help them stick to host tissue, stay intact, and pull in nutrients.
- Fields
Biochemistry
Microbiology & Immunology
Biophysics
- Topics
Corynebacterium diphtheriae
Staphylococcus aureus
Gram-positive bacteria
- Grants
- 2 known grants, through Jun 2029
What they work on
- Determine how the C. diphtheriae surface receptor HbpA captures human hemoglobin, and test whether it works with other heme-binding receptors to distort hemoglobin and trigger heme release.
- Define how Conserved Region domains, heme-binding modules common in Actinobacteria, pass heme across the cell wall by forming low-affinity transfer complexes.
- Use mass spectrometry proteomics and a new fluorogenic hemoglobin reporter to measure the abundance, location, and contribution of each heme-uptake component in live bacteria, testing whether they form a molecular wire to the membrane.
- Learn how pilus polymerases select pilin subunits and crosslink them with lysine-isopeptide bonds to build the SpaA pilus of C. diphtheriae, and solve the first atomic-level structure of a crosslinked pilus.
- Screen chemical libraries of more than 200,000 small molecules with a cell-based assay to find inhibitors of cell wall glycopolymer synthesis in MRSA that could restore sensitivity to β-lactam antibiotics.
More about the research
The research asks how these Gram-positive bacteria build and use their cell surface at the molecular level. It follows two linked threads: how bacteria steal iron from human blood, and how they assemble surface polymers such as hair-like pili and sugar-based glycopolymers. Both threads point toward new ways to fight antibiotic-resistant infections.
Why it matters
Drug-resistant bacterial infections, such as those caused by MRSA, need new treatments. Compounds that block glycopolymer assembly could weaken MRSA's ability to cause infection and make it sensitive again to existing β-lactam antibiotics like penicillin-type drugs. Understanding how pathogens import heme-iron could also reveal targets for therapies that starve bacteria of iron.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Katharine Watts
California Polytechnic State University-San Luis Obispo, CA·Biochemistry
Identify the role of individual genes in TLN-05220 biosynthesis by making gene knockouts in the wild-type bacterium that naturally produces this Echinosporamicin-type antibiotic.
Lilly Immergluck
Morehouse School of Medicine, GA·Public Health & Epidemiology
Apply association mining to antibiotic resistance phenotypes of community-onset Staphylococcus aureus from children to identify which resistance patterns co-occur and how multidrug-resistant profiles have changed over two decades.
Zhaomin Yang
Virginia Polytechnic Institute and State University, VA·Microbiology & Immunology
Improve the potency and selectivity of a novel small-molecule inhibitor of the bacterial type IV pilus through structure–activity relationship studies that systematically vary its chemical structure.
The school
University of California-Los Angeles: 84 labs on PI Pages, $1.9B a year on research, 803 research doctorates a year.
Reach out
A start for your email. Fill in the brackets.