Temporary Membrane Permeabilization via the Pore-Forming Toxin Lysenin

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dc.contributor.authorShrestha, Nisha
dc.contributor.authorThomas, Christopher A.
dc.contributor.authorRichtsmeier, Devon
dc.contributor.authorBogard, Andrew
dc.contributor.authorHermann, Rebecca
dc.contributor.authorWalker, Malyk
dc.contributor.authorAbatchev, Gamid
dc.contributor.authorBrown, Raquel J.
dc.contributor.authorFologea, Daniel
dc.date.accessioned2020-10-08T16:03:51Z
dc.date.available2020-10-08T16:03:51Z
dc.date.copyright2020en_US
dc.date.issued2020
dc.description.abstractPore-forming toxins are alluring tools for delivering biologically-active, impermeable cargoes to intracellular environments by introducing large conductance pathways into cell membranes. However, the lack of regulation often leads to the dissipation of electrical and chemical gradients, which might significantly a ect the viability of cells under scrutiny. To mitigate these problems, we explored the use of lysenin channels to reversibly control the barrier function of natural and artificial lipid membrane systems by controlling the lysenin’s transport properties. We employed artificial membranes and electrophysiology measurements in order to identify the influence of labels and media on the lysenin channel’s conductance. Two cell culture models: Jurkat cells in suspension and adherent ATDC5 cells were utilized to demonstrate that lysenin channels may provide temporary cytosol access to membrane non-permeant propidium iodide and phalloidin. Permeability and cell viability were assessed by fluorescence spectroscopy and microscopy. Membrane resealing by chitosan or specific media addition proved to be an e ective way of maintaining cellular viability. In addition, we loaded non-permeant dyes into liposomes via lysenin channels by controlling their conducting state with multivalent metal cations. The improved control over membrane permeability might prove fruitful for a large variety of biological or biomedical applications that require only temporary, non-destructive access to the inner environment enclosed by natural and artificial membranes.en_US
dc.description.reviewstatusRevieweden_US
dc.description.scholarlevelFacultyen_US
dc.description.sponsorshipThe ATDC5 cells (Sigma Aldrich #99072806) were kindly provided by the Biomolecular Research Center at Boise State University. This research was funded by the National Science Foundation, grant number 1554166, and National Institute of Health (grant numbers P20GM103408 and P20GM109095).en_US
dc.identifier.citationShrestha, N., Thomas, C. A., Richtsmeier, D., Bogard, A., Hermann, R., Walker, M. Abatchev, G., Brown, R. J., & Fologea, D. (2020). Temporary Membrane Permeabilization via the Pore-Forming Toxin Lysenin. Toxins, 12(5), 1-17. https://doi.org/10.3390/toxins12050343.en_US
dc.identifier.urihttps://doi.org/10.3390/toxins12050343
dc.identifier.urihttp://hdl.handle.net/1828/12183
dc.language.isoenen_US
dc.publisherToxinsen_US
dc.subjectlysenin
dc.subjectpermeabilization
dc.subjectpore forming toxins
dc.subjectchitosan
dc.subject.departmentDepartment of Physics and Astronomy
dc.titleTemporary Membrane Permeabilization via the Pore-Forming Toxin Lyseninen_US
dc.typeArticleen_US

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