| Autor: |
Shifrin DA Jr; Department of Cell and Developmental Biology; Vanderbilt University Medical Center; Nashville, TN USA., Crawley SW; Department of Cell and Developmental Biology; Vanderbilt University Medical Center; Nashville, TN USA., Grega-Larson NE; Department of Cell and Developmental Biology; Vanderbilt University Medical Center; Nashville, TN USA., Tyska MJ; Department of Cell and Developmental Biology; Vanderbilt University Medical Center; Nashville, TN USA. |
| Jazyk: |
angličtina |
| Zdroj: |
Gut microbes [Gut Microbes] 2014 Jul 01; Vol. 5 (4), pp. 504-16. Date of Electronic Publication: 2014 Jul 30. |
| DOI: |
10.4161/gmic.32084 |
| Abstrakt: |
Enteropathogenic Escherichia coli (EPEC) induces dramatic remodeling of enterocyte brush borders, a process that includes microvillar effacement and actin pedestal formation. Although the Arp2/3 complex is involved in formation of a branched actin network within pedestals, the fate of parallel actin bundles in microvilli during infection remains unclear. Here, we find that in polarized intestinal epithelial cells, EPEC stimulates long-range microvillar dynamics, pulling protrusions toward sites of bacterial attachment in a process mediated by the adhesion molecule protocadherin-24. Additionally, retraction of the EPEC bundle forming pilus stimulates directed elongation of nearby microvilli. These processes lead to coalescence of microvilli and incorporation of the underlying parallel actin bundles into pedestals. Furthermore, stabilization of microvillar actin bundles delays pedestal formation. Together, these results suggest a model where EPEC takes advantage of pre-existing actin filaments in microvillar core bundles to facilitate pedestal formation. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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