Journal
GUT MICROBES
Volume 5, Issue 4, Pages 504-516Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/gmic.32084
Keywords
microvilli; brush border; EPEC; intestine; espin; bundle forming pilus; Caco-2(BBE)
Categories
Funding
- American Heart Association (AHA)
- National Institutes of Health [DK075555, DK095811]
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK095811, P30DK058404, R01DK075555, R56DK095811] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [T32GM008554] Funding Source: NIH RePORTER
- OFFICE OF THE DIRECTOR, NATIONAL INSTITUTES OF HEALTH [S10OD012324] Funding Source: NIH RePORTER
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Enteropathogenic Escherichia coil (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.
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