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Spatial and Temporal Analysis of Active ERK in the C. elegans Germline
08:40

Spatial and Temporal Analysis of Active ERK in the C. elegans Germline

Published on: November 29, 2016

ERK and RSK regulate distinct steps of a cellular program that induces transition from multicellular epithelium to

Josef Čáslavský1, Zuzana Klímová, Tomáš Vomastek

  • 1Institute of Microbiology, Academy of Sciences of the Czech Republic, Videňská 1083, Prague, Czech Republic.

Cellular Signalling
|September 10, 2013
PubMed

Insights

Extracellular signal-regulated kinases (ERK) and p90 ribosomal S6 kinases (RSK) coordinate epithelial cell changes. ERK triggers polarity loss, while RSK promotes migration, revealing distinct roles in cellular responses.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Signal Transduction

Background:

  • The extracellular signal-regulated kinases (ERK) cascade is a conserved signaling pathway regulating diverse cellular functions.
  • p90 ribosomal S6 kinases (RSKs) are downstream effectors of ERK signaling, but their coordinated roles with ERK are not fully understood.

Purpose of the Study:

  • To investigate the distinct and coordinated roles of ERK and RSK in epithelial cell phenotypic conversion.
  • To elucidate the sequential steps and molecular mechanisms involved in ERK-induced epithelial cell migration.

Main Methods:

  • Conditional activation of the ERK pathway in epithelial cells.
  • Analysis of cellular polarity, cell-cell contact, and migration.
  • Investigation of the role of calpain and actin cytoskeleton remodeling.

Main Results:

  • ERK activation, independent of RSK, induces loss of apical-basal polarity via calpain-mediated actin remodeling.
  • RSK activation is essential for the subsequent stages of cell-cell contact weakening and increased migration.
  • ERK and RSK regulate distinct cellular subprograms in a coordinated temporal manner.

Conclusions:

  • ERK and RSK function sequentially to drive epithelial cell phenotypic conversion to autonomously migrating cells.
  • The biological response to ERK pathway activation is orchestrated by the coordinated actions of ERK and RSK, not a single effector.
  • This study highlights a distributed mechanism for ERK pathway-mediated cellular responses.
Keywords:
4-hydroxytamoxifen4HTALLMALLNCalpainCell–cell junctionsEMTERMAPK/ERKMDCKMadin–Darby Canine KidneyMigrationN-Acetyl-l-leucine-l-leucine-l-norleucinalN-Acetyl-l-leucyl-l-leucyl-l-methionalPolarityRSKepithelial–mesenchymal transitionligand binding domain of estrogen receptor

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