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The JAK-STAT Signaling Pathway01:20

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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
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A feedforward loop between JAK/STAT downstream target p115 and STAT in germline stem cells.

Ruiyan Kong1, Juan Li1, Fuli Liu1

  • 1College of Life Sciences, Capital Normal University, Beijing 100048, China.

Stem Cell Reports
|September 8, 2023
PubMed
Summary

Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling maintains male germline stem cell (GSC) fate. This study identifies p115 as a key downstream target, revealing a feedforward loop essential for GSC maintenance.

Keywords:
Dam-IDDrosophilaJAK/STATStat92Edownstream targetgermline stem cellmaintenancep115spindle orientationtestis

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Area of Science:

  • Developmental Biology
  • Cell Biology
  • Stem Cell Biology

Background:

  • Germline stem cells (GSCs) are crucial for tissue homeostasis.
  • Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling is known to maintain GSC fate in Drosophila testes.
  • The precise downstream mechanisms by which JAK/STAT signaling regulates male GSC fate are not fully understood.

Purpose of the Study:

  • To identify downstream targets of JAK/STAT signaling involved in maintaining male GSC fate.
  • To elucidate the role of the identified target in GSC maintenance and its relationship with JAK/STAT signaling.

Main Methods:

  • Identification of p115 as a putative downstream target of JAK/STAT signaling.
  • Analysis of p115 localization and function in germline cells using microscopy and depletion studies.
  • Investigation of the interaction between p115 and STAT, and the effect of p115 depletion on STAT stability.
  • Assessment of GSC loss and restoration through ectopic STAT expression.

Main Results:

  • p115, a tER/cis-Golgi golgin protein, was identified as a downstream target of JAK/STAT signaling.
  • p115 is localized in the cytosol, ER, and Golgi apparatus, and is essential for their morphology.
  • Depletion of p115 in GSCs leads to aberrant spindle orientation and GSC loss.
  • p115 directly associates with and stabilizes STAT, and ectopic STAT expression rescues GSC loss.

Conclusions:

  • JAK/STAT signaling and p115 form a feedforward loop to maintain male GSC fate.
  • p115 plays a critical role in GSC maintenance by stabilizing STAT and ensuring proper cell morphology and division.
  • This study provides novel insights into the regulatory mechanisms controlling stem cell maintenance via JAK/STAT signaling.