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A single progenitor population switches behavior to maintain and repair esophageal epithelium.

ABSTRACT: Diseases of the esophageal epithelium (EE), such as reflux esophagitis and cancer, are rising in incidence. Despite this, the cellular behaviors underlying EE homeostasis and repair remain controversial. Here, we show that in mice, EE is maintained by a single population of cells that divide stochastically to generate proliferating and differentiating daughters with equal probability. In response to challenge with all-trans retinoic acid (atRA), the balance of daughter cell fate is unaltered, but the rate of cell division increases. However, after wounding, cells reversibly switch to producing an excess of proliferating daughters until the wound has closed. Such fate-switching enables a single progenitor population to both maintain and repair tissue without the need for a "reserve" slow-cycling stem cell pool.

SUBMITTER: Doupe DP

PROVIDER: S-EPMC3527005 | biostudies-literature | 2012 Aug

REPOSITORIES: biostudies-literature

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A single progenitor population switches behavior to maintain and repair esophageal epithelium.

Doupé David P DP Alcolea Maria P MP Roshan Amit A Zhang Gen G Klein Allon M AM Simons Benjamin D BD Jones Philip H PH

Science (New York, N.Y.) 20120719 6098

Diseases of the esophageal epithelium (EE), such as reflux esophagitis and cancer, are rising in incidence. Despite this, the cellular behaviors underlying EE homeostasis and repair remain controversial. Here, we show that in mice, EE is maintained by a single population of cells that divide stochastically to generate proliferating and differentiating daughters with equal probability. In response to challenge with all-trans retinoic acid (atRA), the balance of daughter cell fate is unaltered, bu ...[more]

PMID: 22821983

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