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Induction and Diagnosis of Tumors in Drosophila Imaginal Disc Epithelia
08:14

Induction and Diagnosis of Tumors in Drosophila Imaginal Disc Epithelia

Published on: July 25, 2017

Human homologue of the Drosophila melanogaster lats tumour suppressor modulates CDC2 activity

W Tao1, S Zhang, G S Turenchalk

  • 1Howard Hughes Medical Institute, Department of Genetics, Yale University School of Medicine, Boyer Center for Molecular Medicine, New Haven, Connecticut 06536-0812, USA.

Nature Genetics
|February 13, 1999
PubMed

Insights

The large tumor suppressor (LATS) gene in flies, when mutated, causes tumors and developmental defects. Its human homolog, LATS1, also suppresses tumor growth and rescues these fly defects, indicating conserved functions in cell proliferation.

Area of Science:

  • Cell Biology
  • Genetics
  • Developmental Biology

Background:

  • Mosaic flies serve as models for cancer, mimicking chimaeric patients with mutated somatic cells.
  • The Drosophila melanogaster large tumor suppressor (LATS) gene, a serine/threonine kinase, was identified as a tumor suppressor.
  • Mutations in LATS lead to uncontrolled cell proliferation, tumor formation, and developmental defects, including embryonic lethality.

Purpose of the Study:

  • To investigate the relevance of Drosophila tumor suppressor genes to mammalian tumorigenesis.
  • To isolate and characterize mammalian homologues of the Drosophila LATS gene.
  • To determine the function of mammalian LATS1 in cell cycle regulation and tumor suppression.

Main Methods:

  • Screening of mosaic flies to identify tumor suppressors.
  • Isolation and characterization of mammalian homologues of Drosophila LATS.
  • Analysis of LATS1 phosphorylation and complex formation with CDC2 in mammalian cells.
  • Genetic interaction studies in Drosophila to analyze the function of LATS.

Main Results:

  • Human LATS1 was isolated and found to suppress tumor growth in flies.
  • LATS1 rescued developmental defects and embryonic lethality in Drosophila mutants.
  • Mammalian LATS1 exhibits cell-cycle-dependent phosphorylation and complexes with CDC2, inhibiting its kinase activity.
  • Drosophila lats mutant cells accumulate cyclin A, indicating LATS negatively regulates the CDC2/cyclin A complex.

Conclusions:

  • The Drosophila LATS gene and its human homologue LATS1 are conserved negative regulators of cell proliferation.
  • LATS1 plays a crucial role in cell cycle control and tumor suppression, conserved across species.
  • LATS functions by negatively regulating the CDC2/cyclin A complex, a key component of cell cycle progression.

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