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Title: Targeted deletion of Atg5 reveals differential roles of autophagy in keratin K5-expressing epithelia
Authors: Sukseree S.
Rossiter H.
Mildner M.
Pammer J.
Buchberger M.
Gruber F.
Watanapokasin R.
Tschachler E.
Eckhart L.
Keywords: autophagy protein 5
cell nucleus DNA
cre recombinase
keratin k5
protein p62
unclassified drug
animal experiment
animal tissue
cell differentiation
cell structure
controlled study
DNA degradation
epithelium cell
gene deletion
gene expression
immunofluorescence test
nick end labeling
priority journal
promoter region
reverse transcription polymerase chain reaction
weight gain
Western blotting
Body Weight
Cell Differentiation
Epithelial Cells
Gene Deletion
Gene Targeting
Mice, Transgenic
Microtubule-Associated Proteins
Thymus Gland
Weight Gain
Issue Date: 2013
Abstract: Autophagy contributes to the homeostasis of many tissues, yet its role in epithelia is incompletely understood. A recent report proposed that Atg5-dependent autophagy in thymic epithelial cells is essential for their function in the negative selection of self-reactive T-cells and, thus, for the suppression of tissue inflammation. Here we crossed mice carrying floxed alleles of the Atg5 gene with mice expressing the Cre recombinase under the control of the keratin K5 promoter to suppress autophagy in all K5-positive epithelia. The efficiency of autophagy abrogation was confirmed by immunoanalyses of LC3, which was converted to the autophagy-associated LC3-II form in normal but not Atg5-deficient cells, and of p62, which accumulated in Atg5-deficient cells. Mice carrying the epithelium-specific deletion of Atg5 showed normal weight gain, absence of tissue inflammation, and a normal morphology of the thymic epithelium. By contrast, autophagy-deficient epithelial cells of the preputial gland showed aberrant eosinophilic staining in histology and premature degradation of nuclear DNA during terminal differentiation. Taken together, the results of this study suggest that autophagy is dispensable for the suppression of autoimmunity by thymic epithelial cells but essential for normal differentiation of the preputial gland in mice. © 2012 Elsevier Inc.
ISSN: 0006291X
Appears in Collections:SCOPUS 1983-2021

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