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BMI1 represses Ink4a/Arf and Hox genes to regulate stem cells in the rodent incisor
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BMI1 represses Ink4a/Arf and Hox genes to regulate stem cells in the rodent incisor
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Journal Article
BMI1 represses Ink4a/Arf and Hox genes to regulate stem cells in the rodent incisor
2013
Overview
The polycomb protein BMI1 has been linked to maintenance of adult stem cells. Klein and colleagues find that BMI1 is also required for the maintenance of stem cells in the continuously growing mouse incisor, through repression of the
Ink4a/Arf
locus to modulate the proliferation of stem cells and repression of
Hox
genes to prevent inappropriate lineage decisions in stem cell progeny.
The polycomb group gene
Bmi1
is required for maintenance of adult stem cells in many organs
1
,
2
. Inactivation of
Bmi1
leads to impaired stem cell self-renewal due to deregulated gene expression. One critical target of BMI1 is
Ink4a/Arf
, which encodes the cell-cycle inhibitors p16
Ink4a
and p19
Arf
(ref.
3
). However, deletion of
Ink4a/Arf
only partially rescues
Bmi1
-null phenotypes
4
, indicating that other important targets of BMI1 exist. Here, using the continuously growing mouse incisor as a model system, we report that
Bmi1
is expressed by incisor stem cells and that deletion of
Bmi1
resulted in fewer stem cells, perturbed gene expression and defective enamel production. Transcriptional profiling revealed that
Hox
expression is normally repressed by BMI1 in the adult, and functional assays demonstrated that BMI1-mediated repression of
Hox
genes preserves the undifferentiated state of stem cells. As
Hox
gene upregulation has also been reported in other systems when
Bmi1
is inactivated
1
,
2
,
5
,
6
,
7
, our findings point to a general mechanism whereby BMI1-mediated repression of
Hox
genes is required for the maintenance of adult stem cells and for prevention of inappropriate differentiation.
Publisher
Nature Publishing Group UK,Nature Publishing Group
