Notch signalling maintains
intestinal stem cells


In addition to repressing the
secretory cell phenotype, notch signalling has been implicated in maintaining
the proliferative state of intestinal progenitors and stem cells.

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Co-localisation of Hes1, with the intestinal stem cell marker Musashi-1 (Msi1)
in cells at the bottom of the crypt, indicated the presence of notch activity
in CBC’s. A similar observation was made at the +4 stem cells in the small
intestine. Lineage tracing studies using a tamoxifen induced Notch1 Cre-mouse
model (NIP1::CreERT2) revealed that, after eight months, labelled
cells occupied the entire crypt (and villus) and expressed markers of all the
differentiated cell types in the adult intestine (Pellegrinet et al, 2012).  This showed that cells expressing Notch1
activity were capable of self-renewal and differentiation, therefore,
expressing stem-cell properties. A lower number of Notch1 labelled cells were
found in the colon as compared to the small intestine. This phenomenon is
similar to the aforementioned observation in Lgr5 lineage tracing experiments,
where slower cycling rates were attributed to colonic CBC’s (Barker et
al,2007). The discovery of Lgr5 as a unique marker of CBC’s paved way for the identification
of Notch activity in intestinal stem cells as well. Dll1 and Dll4 double knockout
and RBP-J inactivated mice, along with increased goblet cell numbers, lost the
expression of stem cell markers including Lgr5, Olfm4 and Ascl2. Furthermore,
proliferating Ki67-positive cells in the crypts were ablated (Pellegrinet et
al, 2012). 


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