The DOI matches its Crossref record; 44 of the 44 references it cites were found in a registry or an index.
Dll1- and Dll4-Mediated Notch Signaling Are Required for Homeostasis of Intestinal Stem Cells
Open accessAbstract
Background & Aims Ablation of Notch signaling within the intestinal epithelium results in loss of proliferating crypt progenitors, due to their conversion into post-mitotic secretory cells. We aimed to confirm that Notch was active in stem cells (SC), investigate consequences of loss of Notch signaling within the intestinal SC compartment, and identify the physiological ligands of Notch in mouse intestine. Furthermore, we investigated whether the induction of goblet cell differentiation that results from loss of Notch requires the transcription factor Krüppel-like factor 4 (Klf4). Methods Trasgenic mice that carried a reporter of Notch1 activation were used for lineage tracing experiments. The in vivo functions of the Notch ligands Jagged1 (Jag1), Delta-like1 (Dll1), Delta-like4 (Dll4), and the transcription factor Klf4 were assessed in mice with inducible, gut-specific gene targeting (Vil-Cre-ERT2). Results Notch1 signaling was found to be activated in intestinal SC. Although deletion of Jag1 or Dll4 did not perturb the intestinal epithelium, inactivation of Dll1 resulted in a moderate increase in number of goblet cells without noticeable effects of progenitor proliferation. However, simultaneous inactivation of Dll1 and Dll4 resulted in the complete conversion of proliferating progenitors into post-mitotic goblet cells, concomitant with loss of SC (Olfm4+, Lgr5+ and Ascl2+). Klf4 inactivation did not interfere with goblet cell differentiation in adult wild-type or in Notch pathway-deficient gut. Conclusions Notch signaling in SC and progenitors is activated by Dll1 and Dll4 ligands and is required for maintenance of intestinal progenitor and SC. Klf4 is dispensable for goblet cell differentiation in intestines of adult Notch-deficient mice.
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Cites
Single Lgr5 stem cells build crypt-villus structures in vitro without a mesenchymal niche
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Self-citationStem Cells, Self-Renewal, and Differentiation in the Intestinal Epithelium
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Self-citationBmi1 is expressed in vivo in intestinal stem cells
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Tissue‐specific and inducible Cre‐mediated recombination in the gut epithelium
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Blockade of Dll4 inhibits tumour growth by promoting non-productive angiogenesis
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Cited by
The intestinal crypt, a prototype stem cell compartment
Clevers, H. (2013) · Cell · doi:10.1016/j.cell.2013.07.004 · Cited by 1,223
Growing Self-Organizing Mini-Guts from a Single Intestinal Stem Cell: Mechanism and Applications
Sato, T., & Clevers, H. (2013) · Science · doi:10.1126/science.1234852 · Cited by 1,170
Paneth Cells: Maestros of the Small Intestinal Crypts
Clevers, H. C., & Bevins, C. L. (2013) · Annual Review of Physiology · doi:10.1146/annurev-physiol-030212-183744 · Cited by 699
Redundant sources of Wnt regulate intestinal stem cells and promote formation of Paneth cells
Farin, H. F., Van Es, J. H., & Clevers, H. (2012) · Gastroenterology · doi:10.1053/j.gastro.2012.08.031 · Cited by 655
VanDussen, K. L., Carulli, A. J., Keeley, T. M., Patel, S. R., Puthoff, B. J., Magness, S. T., Tran, I. T., Maillard, I., Siebel, C., Kolterud, Å., et al. (2012) · Development · doi:10.1242/dev.070763 · Cited by 578
Metadata
- Authors
- Pellegrinet, L., Rodilla, V., Liu, Z., Chen, S., Koch, U., Espinosa, L., Kaestner, K. H., Kopan, R., Lewis, J., & Radtke, F.
- Venue
- Gastroenterology
- Publisher
- Elsevier BV
- Published
- 2011-04
- Volume
- 140
- Issue
- 4
- Pages
- 1230-1240.e7
- ISSN
- 0016-5085 (ISSN-L)
- OpenAlex
- W1969335165
- Cited by
- 431
- References
- 44
- FWCI
- 12.81
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Pellegrinet, L., Rodilla, V., Liu, Z., Chen, S., Koch, U., Espinosa, L., Kaestner, K. H., Kopan, R., Lewis, J., & Radtke, F. (2011). Dll1- and Dll4-Mediated Notch Signaling Are Required for Homeostasis of Intestinal Stem Cells. Gastroenterology. https://doi.org/10.1053/j.gastro.2011.01.005
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