Nathan Wittenberg
Lehigh University, PA·Biophysics·Early-career
Cell membranes are not passive bags; their lipid makeup, electric charge and curvature decide which molecules stick to them and how strongly. Measurements of such binding are usually made on huge populations of membranes at once, which averages away the fact that individual membranes differ from one another.
- Fields
Biophysics
Chemistry
Microbiology & Immunology
- Topics
antimicrobial peptides
outer membrane vesicles
lipopolysaccharide
- Grants
- 2 known grants, through May 2027
What they work on
- Determine how vesicle size, surface charge, lipid saturation and lipopolysaccharide composition control binding of the antimicrobial peptide LL-37, using liposomes of defined composition measured on single vesicles and subpopulations.
- Relate the LL-37 affinity of bacterial outer membrane vesicles sorted by size and charge to how well those vesicles protect bacterial cells from being killed by the peptide.
- Test how the physical and chemical properties of outer membrane vesicles change after bacteria are exposed to LL-37, and whether those changes alter subsequent peptide binding.
- Measure how cholesterol modulates binding between myelin-associated glycoprotein (MAG), a nerve-growth inhibitor, and the sugar-bearing lipids GD1a and GT1b, and the membrane-membrane adhesion that follows, using QCM-D biosensing and FRET.
- Determine how separation of membranes into lipid raft-like domains shapes where and when MAG-ganglioside interactions occur, using total internal reflection fluorescence microscopy and equilibrium fluctuation analysis.
- Test how the composition of the MAG receptor complex (NgR1 with p75 and LINGO-1) sets MAG binding affinity, and how anti-LINGO-1 antibodies disrupt the MAG-NgR1 interaction.
More about the research
Work here develops and applies measurements that resolve binding on single membrane vesicles and on subpopulations, applied to two problems: how bacteria use shed membrane bubbles to blunt antimicrobial attack, and how cholesterol and membrane organization control a nerve protein that blocks nerve regrowth.
Why it matters
Antibiotic resistance makes alternatives like antimicrobial peptides attractive, and knowing which vesicle properties let bacteria neutralize these peptides could inform the design of versions that evade the decoy and remain effective. On the neural side, MAG's grip on neurons is a known obstacle to repair after nervous system injury; understanding how cholesterol, membrane domains and receptor partners tune that grip could point toward ways to release the brake on nerve regrowth.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Isiah Warner
University of Cincinnati, OH·Chemistry
Develop chemical sensors that pair GUMBOS, solid organic salts, with a quartz crystal microbalance so that selective salt–analyte interactions register as measurable signals.
Albert Siryaporn
University of California-Irvine, CA·Microbiology & Immunology
Identify combinations of human histones with the antimicrobial peptide LL-37 and other membrane- or cell wall-targeting antimicrobials that produce the strongest killing and synergy against Staphylococcus aureus, Pseudomonas aeruginosa, and communities of skin bacteria in vitro.
Joseph Falke
University of Colorado Boulder, CO·Biochemistry
Determine how Class 1 and Class 3 PI3K enzymes integrate calcium, receptor and G protein inputs, and whether these combine additively, synergistically or in opposition, using single-molecule TIRF microscopy on supported lipid bilayers.
The school
Lehigh University: 13 labs on PI Pages, $62M a year on research, 99 research doctorates a year.
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