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Citation
Li, Z., Guo, X., Huang, H., Wang, C., Yang, F., Zhang, Y., Wang, J., Han, L., Jin, Z., Cai, T., Xi, R. (2020). A Switch in Tissue Stem Cell Identity Causes Neuroendocrine Tumors in Drosophila Gut.  Cell Rep. 30(6): 1724--1734.e4.
FlyBase ID
FBrf0244831
Publication Type
Research paper
Abstract

Intestinal stem cells (ISCs) are able to generate gut-specific enterocytes, as well as neural-like enteroendocrine cells. It is unclear how the tissue identity of the ISC lineage is regulated to confer cell-lineage fidelity. Here, we show that, in adult Drosophila midgut, loss of the transcriptional repressor Tramtrack in ISCs causes a self-renewal program switch to neural stem cell (NSC)-like, and that switch drives neuroendocrine tumor development. In Tramtrack-depleted ISCs, the ectopically expressed Deadpan acts as a major self-renewal factor for cell propagation, and Sequoia acts as a differentiation factor for the neuroendocrine phenotype. In addition, the expression of Sequoia renders NSC-specific self-renewal genes responsive to Notch in ISCs, thus inverting the differentiation-promoting function of Notch into a self-renewal role as in normal NSCs. These results suggest an active maintenance mechanism for the gut identity of ISCs, whose disruption may lead to an improper acquisition of NSC-like traits and tumorigenesis.

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Erratum

A Switch in Tissue Stem Cell Identity Causes Neuroendocrine Tumors in Drosophila Gut.
Li et al., 2020, Cell Rep. 33(9): 108459 [FBrf0247485]

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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Cell Rep.
    Title
    Cell reports
    ISBN/ISSN
    2211-1247
    Data From Reference