Escargot controls somatic stem cell maintenance through the attenuation of the insulin receptor pathway in Drosophila.

Cell Rep

Department of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA; Laboratory of Genetics, Salk Institute for Biological Studies, La Jolla, CA 92037, USA; Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, University of California, Los Angeles, Los Angeles, CA 90095, USA; Department of Anatomy, Division of Geriatrics, University of California, San Francisco, San Francisco, CA 94143, USA; Department of Medicine, Division of Geriatrics, University of California, San Francisco, San Francisco, CA 94143, USA; Eli and Edythe Broad Center for Regeneration Medicine, University of California, San Francisco, San Francisco, CA 94143, USA. Electronic address:

Published: April 2022

Adult stem cells coordinate intrinsic and extrinsic, local and systemic, cues to maintain the proper balance between self-renewal and differentiation. However, the precise mechanisms stem cells use to integrate these signals remain elusive. Here, we show that Escargot (Esg), a member of the Snail family of transcription factors, regulates the maintenance of somatic cyst stem cells (CySCs) in the Drosophila testis by attenuating the activity of the pro-differentiation insulin receptor (InR) pathway. Esg positively regulates the expression of an antagonist of insulin signaling, ImpL2, while also attenuating the expression of InR. Furthermore, Esg-mediated repression of the InR pathway is required to suppress CySC loss in response to starvation. Given the conservation of Snail-family transcription factors, characterizing the mechanisms by which Esg regulates cell-fate decisions during homeostasis and a decline in nutrient availability is likely to provide insight into the metabolic regulation of stem cell behavior in other tissues and organisms.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9043617PMC
http://dx.doi.org/10.1016/j.celrep.2022.110679DOI Listing

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