Role of the β1-integrin cytoplasmic tail in mediating invasin-promoted internalization of Yersinia
2002 (English)In: Journal of Cell Science, ISSN 0021-9533, E-ISSN 1477-9137, Vol. 115, no 13, 2669-2678 p.Article in journal (Refereed) Published
Invasin of Yersinia pseudotuberculosis binds to beta1-integrins on host cells and triggers internalization of the bacterium. To elucidate the mechanism behind the beta1-integrin-mediated internalization of Yersinia, a beta1-integrin-deficient cell line, GD25, transfected with wild-type beta1A, beta1B or different mutants of the beta1A subunit was used. Both beta1A and beta1B bound to invasin-expressing bacteria, but only beta1A was able to mediate internalization of the bacteria. The cytoplasmic region of beta1A, differing from beta1B, contains two NPXY motifs surrounding a double threonine site. Exchanging the tyrosines of the two NPXYs to phenylalanines did not inhibit the uptake, whereas a marked reduction was seen when the first tyrosine (Y783) was exchanged to alanine. A similar reduction was seen when the two nearby threonines (TT788-9) were exchanged with alanines. It was also noted that cells affected in bacterial internalization exhibited reduced spreading capability when seeded onto invasin, suggesting a correlation between the internalization of invasin-expressing bacteria and invasin-induced spreading. Likewise, integrins defective in forming peripheral focal complex structures was unable to mediate uptake of invasin-expressing bacteria.
Place, publisher, year, edition, pages
2002. Vol. 115, no 13, 2669-2678 p.
Invasin, b1-integrin, Yersinia pseudotuberculosis, Focal complexes, Bacterial internalization
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:umu:diva-3443PubMedID: 12077358OAI: oai:DiVA.org:umu-3443DiVA: diva2:142138