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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
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JAK/STAT signalling mediates cell survival in response to tissue stress

Marco La Fortezza1, Madlin Schenk1, Andrea Cosolo1

  • 1Ludwig-Maximilians-University Munich, Faculty of Biology, Grosshaderner Strasse 2-4, Planegg-Martinsried 82152, Germany.

Development (Cambridge, England)
|July 8, 2016
PubMed

Insights

The Janus kinase/Signal transducers and activators of transcription (JAK/STAT) pathway restrains c-Jun amino-terminal kinase (JNK)-induced apoptosis and promotes cell survival, maintaining tissue homeostasis and limiting damage during stress responses.

Area of Science:

  • Cellular stress response
  • Developmental biology
  • Signaling pathways

Background:

  • Tissue homeostasis depends on stress response mechanisms.
  • The c-Jun amino-terminal kinase (JNK) pathway regulates apoptosis and proliferation following injury.
  • Balancing these opposing responses within a single pathway remains unclear.

Purpose of the Study:

  • Investigate the role of the Janus kinase/Signal transducers and activators of transcription (JAK/STAT) pathway in stress response.
  • Elucidate the crosstalk between JNK and JAK/STAT signaling.
  • Determine how these pathways interact to maintain tissue homeostasis.

Main Methods:

  • Utilized Drosophila melanogaster models for tissue regeneration and tumor studies.
  • Analyzed imaginal discs for JAK/STAT pathway activation upon damage.
  • Investigated the regulatory relationship between JAK/STAT, JNK, and apoptosis-related genes.

Main Results:

  • Demonstrated JAK/STAT pathway activation in damaged imaginal discs.
  • Showed that JAK/STAT signaling promotes survival of JNK-activated cells.
  • Identified JAK/STAT-dependent regulation of JNK component fos and pro-apoptotic gene hid.
  • Confirmed JAK/STAT's role in limiting JNK-induced apoptosis and tumor growth under chronic stress.

Conclusions:

  • The JAK/STAT pathway restrains JNK-mediated apoptosis and controls JNK signaling propagation.
  • This pathway facilitates compensatory proliferation and limits tissue damage.
  • JAK/STAT signaling promotes cell survival, contributing to tumor growth under chronic stress.
  • Interplay between conserved signaling pathways establishes equilibrium for tissue homeostasis.
Keywords:
CancerCell ablationCell survivalCompensatory proliferationEigerInjury-induced apoptosisJAK/STATJNK

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