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


ABSTRACT: 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.

SUBMITTER: Senos Demarco R 

PROVIDER: S-EPMC9043617 | biostudies-literature | 2022 Apr

REPOSITORIES: biostudies-literature

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

Sênos Demarco Rafael R   Stack Brian J BJ   Tang Alexander M AM   Voog Justin J   Sandall Sharsti L SL   Southall Tony D TD   Brand Andrea H AH   Jones D Leanne DL  

Cell reports 20220401 3


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) pathw  ...[more]

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