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Synthetic dysmobility screen unveils an integrated STK40-YAP-MAPK system driving cell migration

Ling-Yea Yu1,2, Ting-Jen Tseng1, Hsuan-Chao Lin3

  • 1Department of Pharmacology, National Taiwan University College of Medicine, Taipei, Taiwan.

Science Advances
|July 29, 2021
PubMed

Insights

Simultaneously suppressing serine-threonine kinase 40 (STK40) and mitogen-activated protein kinase (MAPK) synergistically reduces cell migration. This reveals a novel STK40-YAP-MAPK pathway controlling cell motility and focal adhesion dynamics.

Area of Science:

  • Cell biology
  • Molecular biology
  • Biochemistry

Background:

  • Cell survival relies on integrating signals, leading to synthetic lethality.
  • Mechanisms of signaling integration controlling cell migration are not fully understood.

Purpose of the Study:

  • To investigate how signaling pathways are integrated to regulate cell migration.
  • To identify novel molecular targets for controlling cell motility.

Main Methods:

  • Conducted a "two-hit" genetic screen to identify synergistic interactions affecting cell migration.
  • Utilized single-cell analyses to assess cell motility, focal adhesion dynamics, and protein localization.
  • Investigated the roles of serine-threonine kinase 40 (STK40), yes-associated protein (YAP), and mitogen-activated protein kinase (MAPK) in cell migration.

Main Results:

  • Simultaneous suppression of STK40 and MAPK synergistically reduced cell migration.
  • STK40 knockdown enhanced focal adhesion complex stability, reducing cell motility and coordination.
  • STK40 knockdown destabilized YAP, decreasing nuclear transport, while MAPK inhibition further impaired nuclear YAP activity and focal adhesion remodeling.

Conclusions:

  • Unveiled an integrated STK40-YAP-MAPK signaling system that regulates cell migration.
  • Introduced "synthetic dysmobility" as a novel strategy targeting this pathway to control cell migration.

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