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Updated: Aug 16, 2026

Monitoring Hippo Signaling Pathway Activity Using a Luciferase-based Large Tumor Suppressor (LATS) Biosensor
07:16

Monitoring Hippo Signaling Pathway Activity Using a Luciferase-based Large Tumor Suppressor (LATS) Biosensor

Published on: September 13, 2018

Human LATS1 is a mitotic exit network kinase

John Bothos1, Robyn L Tuttle, Michelle Ottey

  • 1The Wistar Institute, Philadelphia, PA 19104-4268, USA.

Cancer Research
|August 3, 2005
PubMed

Insights

The tumor suppressor LATS1 kinase interacts with MOB1A, revealing a role in mitotic exit. This finding explains LATS1

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • The tumor suppressor kinase LATS1/WARTS is evolutionarily conserved, yet its precise molecular functions remain largely unknown.
  • Understanding LATS1's role is crucial for comprehending tumor suppression mechanisms and cell cycle regulation.

Purpose of the Study:

  • To investigate the molecular function of human LATS1 and identify its interaction partners.
  • To determine if LATS1 plays a role in the mitotic exit network in higher eukaryotes.

Main Methods:

  • Co-immunoprecipitation to identify LATS1 interacting proteins.
  • Cellular assays involving LATS1/MOB1A overexpression and small interfering RNA (siRNA) knockdown.
  • Microscopy to assess the effects on mitotic progression, specifically telophase duration.

Main Results:

  • Human LATS1 was found to interact with MOB1A, a protein linked to mitotic exit kinases in yeast.
  • Overexpression of LATS1 accelerated mitotic exit in cells treated with microtubule poisons, an effect dependent on MOB1A.
  • Suppression of LATS1 or MOB1A using siRNA prolonged telophase without affecting earlier mitotic stages.

Conclusions:

  • LATS1 is a component of the mitotic exit network in higher eukaryotes, functioning in conjunction with MOB1A.
  • The identified role of LATS1 in mitotic exit provides a molecular explanation for its previously observed functions in G2 arrest and cytokinesis promotion.

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