Role of the Adherens Junction Protein Fascin in the Regulation of Tight Junction Permeability in the Mouse Mammary Gland
Abstract
An adenovirus gene delivery system was developed allowing target gene delivery to the mouse mammary gland and cultured cells. This system was used to express a truncation mutant of the tight junction protein occludin in the mouse mammary gland and in cultured epithelial cells. The expression of truncated occludin caused programmed cell death in the mouse mammary gland epithelium and in cultured epithelial cells. Occludin and the apical junction complex proteins ZO-1 and beta-catenin left the tight junction following transgene expression. The beta-catenin binding, actin remodeling protein fascin was upregulated in transgene expression cells. The fluorescent staining of fascin was brilliant and cytoplasmically diffuse. Fascin upregulation was proposed to be an inherent part of the programmed cell death process. Recent work demonstrated an upregulation of fascin during cell death downstream of topoisomerase inhibition. That fascin is apparently upregulated downstream of such divergent apoptotic stimuli as loss of cell/cell contact and DNA strand breaks suggests that actin plays a fundamental role in apoptosis. The apical junction proteins beta-catenin, AF-6 and P-120 thought to interact molecularly with fascin, were shown to leave the apical junction complex and distribute to the perinuclear region. Monomeric actin was shown to increase during apoptosis.
Document Details
- Document Type
- Technical Report
- Publication Date
- Aug 01, 2003
- Accession Number
- ADA423862
Entities
People
- Margaret Neville
- Neal E. Beeman
Organizations
- University of Colorado Health