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Cell Lineage metastability in Gfi1-deficient mouse intestinal epithelium.

Matthew Bjerknes¹, Hazel Cheng

¹Department of Medicine, Clinical Science Division, Medical Sciences Building, Room 6334, University of Toronto, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8. matthew.bjerknes@utoronto.ca

Developmental Biology

|July 6, 2010

Summary

The zinc-finger transcriptional repressor Gfi1 normally represses Neurog3 in mucous and Paneth intestinal cells. Gfi1 deficiency causes these cells to reprogram into enteroendocrine cells, explaining altered cell proportions.

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Area of Science:

Cell Biology
Developmental Biology
Genetics

Background:

Multipotent progenitor cell fate determination is crucial in biology.
Defects in the zinc-finger transcriptional repressor Gfi1 cause significant changes in differentiated cell types.
Gfi1-deficient intestinal epithelium shows a shift from mucous and Paneth cells towards enteroendocrine cells.

Purpose of the Study:

Investigate the mechanisms behind the Gfi1-deficient intestinal phenotype.
Determine the role of Gfi1 in regulating intestinal cell fate.
Clarify the proposed common granulocytic progenitor model.

Main Methods:

Analysis of Gfi1 expression in mouse intestinal epithelium.
Investigation of Neurog3 expression in Gfi1-deficient crypt cells.
Observation of cellular reprogramming in Gfi1-deficient intestinal lineages.

Main Results:

Mucous and Paneth lineage cells normally express Gfi1.
Gfi1-deficient mice show aberrant Neurog3 expression in sporadic mucous and Paneth cells.
Mucous and Paneth cells exhibit reprogramming into enteroendocrine cells in Gfi1-deficient mice.

Conclusions:

Gfi1 is required for stable repression of Neurog3 in mucous and Paneth lineages.
Lineage metastability of mucous and Paneth cells explains the observed cell proportion shifts.
The Gfi1-deficient phenotype is due to reprogramming, not reallocation from a common progenitor.