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ID1 is a functional marker for intestinal stem and progenitor cells required for normal response to injury.

TitleID1 is a functional marker for intestinal stem and progenitor cells required for normal response to injury.
Publication TypeJournal Article
Year of Publication2014
AuthorsZhang N, Yantiss RK, Nam H-S, Chin Y, Zhou XKathy, Scherl EJ, Bosworth BP, Subbaramaiah K, Dannenberg AJ, Benezra R
JournalStem Cell Reports
Date Published2014 Nov 11
KeywordsAnimals, Biomarkers, Cell Proliferation, Colitis, Colon, Dextran Sulfate, Gene Expression, Humans, Immunohistochemistry, Inhibitor of Differentiation Protein 1, Intestinal Mucosa, Intestines, Ki-67 Antigen, Mice, Inbred C57BL, Mice, Inbred Strains, Mice, Knockout, Mice, Transgenic, Multipotent Stem Cells, Organoids, Receptors, G-Protein-Coupled, Reverse Transcriptase Polymerase Chain Reaction

LGR5 and BMI1 mark intestinal stem cells in crypt base columnar cells and +4 position cells, respectively, but characterization of functional markers in these cell populations is limited. ID1 maintains the stem cell potential of embryonic, neural, and long-term repopulating hematopoietic stem cells. Here, we show in both human and mouse intestine that ID1 is expressed in cycling columnar cells, +4 position cells, and transit-amplifying cells in the crypt. Lineage tracing revealed ID1+ cells to be self-renewing, multipotent stem/progenitor cells that are responsible for the long-term renewal of the intestinal epithelium. Single ID1+ cells can generate long-lived organoids resembling mature intestinal epithelium. Complete knockout of Id1 or selective deletion of Id1 in intestinal epithelium or in LGR5+ stem cells sensitizes mice to chemical-induced colon injury. These experiments identify ID1 as a marker for intestinal stem/progenitor cells and demonstrate a role for ID1 in maintaining the potential for repair in response to colonic injury.

Alternate JournalStem Cell Reports
PubMed ID25418719
PubMed Central IDPMC4235234
Grant ListP30 CA008748 / CA / NCI NIH HHS / United States