Open AccessBrief Report: Dclk1 Deletion in Tuft Cells Results in Impaired Epithelial Repair After Radiation Injury
Author(s) -
May Randal,
Q Dongfeng,
Weygant Nathaniel,
Chandrakesan Parthasarathy,
Ali Naushad,
Lightfoot Stanley A.,
Li Linheng,
Sureban Sripathi M.,
Houchen Courtney W.
Publication year - 2014
Publication title -
stem cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.159
H-Index - 229
eISSN - 1549-4918
pISSN - 1066-5099
DOI - 10.1002/stem.1566
Subject(s) - crypt , biology , stem cell , microbiology and biotechnology , villin , epithelium , intestinal epithelium , intestinal mucosa , tuft , cancer research , immunology , pathology , genetics , medicine , endocrinology , actin , materials science , composite material
The role of Dclk1 + tuft cells in the replacement of intestinal epithelia and reestablishing the epithelial barrier after severe genotoxic insult is completely unknown. Successful restoration requires precise coordination between the cells within each crypt subunit. While the mechanisms that control this response remain largely uncertain, the radiation model remains an exceptional surrogate for stem cell‐associated crypt loss. Following the creation of Dclk1‐intestinal‐epithelial‐deficient Villin‐Cre;Dclk1 flox/flox mice, widespread gene expression changes were detected in isolated intestinal epithelia during homeostasis. While the number of surviving crypts was unaffected, Villin‐Cre;Dclk1 flox/flox mice failed to maintain tight junctions and died at approximately 5 days, where Dclk1 flox/flox mice lived until day 10 following radiation injury. These findings suggest that Dclk1 plays a functional role critical in the epithelial restorative response. S tem C ells 2014;32:822–827