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Constitutively active RAS prolongs Cdc42 signalling, while MAPK signalling is attenuated during fission yeast mating.

Emma J Kelsall1, Akatsuki Kimura2,3,4, Ábel Vértesy5

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Fission yeast RAS mutations differentially activate Cdc42 and MAPKSpk1 pathways. A mathematical model revealed a negative-feedback circuit crucial for regulating MAPKSpk1 signalling dynamics in this RAS signalling network.

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Area of Science:

  • Cellular signalling
  • Molecular biology
  • Systems biology

Background:

  • RAS GTPases are key signalling hubs controlling diverse cellular processes.
  • RAS-mediated signalling can activate multiple downstream pathways, potentially with differential responses to mutations.
  • Fission yeast pheromone signalling (PS) involves RAS signalling, activating both the MAPKSpk1 and Cdc42 pathways.

Purpose of the Study:

  • To investigate how a constitutively active RAS mutation (ras1.G17V) differentially affects downstream MAPKSpk1 and Cdc42 pathway activation in fission yeast.
  • To elucidate the network structure governing RAS-mediated pheromone signalling, particularly the transient activation of MAPKSpk1.
  • To develop and validate a mathematical model of the fission yeast pheromone signalling framework.

Main Methods:

  • Genetic epistasis analysis of pheromone signalling mutants.
  • Biochemical analysis of Ras1 effectors (Cdc42-GEFScd1 and MAPKKKByr2).
  • Development of a mathematical model based on the pheromone signalling framework.
  • Experimental validation of model predictions, including gene deletions (e.g., Sxa2).

Main Results:

  • The ras1.G17V mutation caused prolonged Cdc42 activation but transient MAPKSpk1 activation.
  • Ras1 signalling branches into MAPKSpk1 and Cdc42 pathways, with competitive interaction between effectors.
  • A negative-feedback circuit regulating pheromone production/sensing was identified as essential for explaining MAPKSpk1 dynamics.
  • Experimental deletion of Sxa2 confirmed the predicted negative-feedback, leading to hyperactivation of both pathways.

Conclusions:

  • RAS signalling propagates distinctly through the MAPKSpk1 and Cdc42 pathways in fission yeast.
  • A negative-feedback mechanism is critical for controlling the transient activation of the MAPKSpk1 pathway.
  • The developed mathematical model provides a framework for understanding RAS signalling networks and can be adapted for other systems.