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Diphtheria toxin translocation across cellular membranes is regulated by sphingolipids.

Abstract：

:Diphtheria toxin is translocated across cellular membranes when receptor-bound toxin is exposed to low pH. To study the role of sphingolipids for toxin translocation, both a mutant cell line lacking the first enzyme in de novo sphingolipid synthesis, serine palmitoyltransferase, and a specific inhibitor of the same enzyme, myriocin, were used. The serine palmitoyltransferase-deficient cell line (LY-B) was found to be 10-15 times more sensitive to diphtheria toxin than the genetically complemented cell line (LY-B/cLCB1) and the wild-type cell line (CHO-K1), both when toxin translocation directly across the plasma membrane was induced by exposing cells with surface-bound toxin to low pH, and when the toxin followed its normal route via acidified endosomes into the cytosol. Toxin binding was similar in these three cell lines. Furthermore, inhibition of serine palmitoyltransferase activity by addition of myriocin sensitized the two control cell lines (LY-B/cLCB1 and CHO-K1) to diphtheria toxin, whereas, as expected, no effect was observed in cells lacking serine palmitoyltransferase (LY-B). In conclusion, diphtheria toxin translocation is facilitated by depletion of membrane sphingolipids.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Spilsberg B,Hanada K,Sandvig K

doi

10.1016/j.bbrc.2005.02.005

subject

Has Abstract

pub_date

2005-04-08 00:00:00

pages

465-73

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(05)00231-7

journal_volume

329

pub_type

杂志文章

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