Related Experiment Video

Updated: Sep 23, 2025

Sonication-facilitated Immunofluorescence Staining of Late-stage Embryonic and Larval Drosophila Tissues In Situ
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Regulation of developmental hierarchy in Drosophila neural stem cell tumors by COMPASS and Polycomb complexes

Cassandra Gaultier1, Sophie Foppolo1, Cédric Maurange1

  • 1Aix Marseille University, CNRS, IBDM, Turing Centre for Living systems, Equipe Labellisée Ligue Contre le Cancer, Campus de Luminy Case 907, 13288 Cedex 09 Marseille, France.

Science Advances
|May 11, 2022
PubMed

Insights

Inactivating COMPASS and Polycomb complexes in Drosophila neuroblast tumors disrupts cellular hierarchy, expanding cancer stem cells (CSCs). This study reveals how these chromatin complexes impact tumor growth and CSC plasticity.

Area of Science:

  • Developmental Biology
  • Cancer Biology
  • Chromatin Biology

Background:

  • COMPASS and Polycomb complexes are antagonistic chromatin regulators often inactivated in cancers.
  • Their role in tumor hierarchy, composition, and growth remains poorly understood.
  • Drosophila neuroblast tumors provide a model to study cancer stem cell (CSC) properties driven by temporal patterning.

Purpose of the Study:

  • To investigate how COMPASS and Polycomb complex inactivation affects tumor hierarchy and CSCs in Drosophila.
  • To elucidate the mechanisms by which these complexes regulate developmental trajectories in cancer.

Main Methods:

  • Single-cell transcriptomics was employed to analyze tumor composition and cellular states.
  • Genetic manipulation (trithorax knockdown, Polycomb repressive complex 2 inactivation) was used to study gene function.

Main Results:

  • The trithorax/MLL1/2-COMPASS-like complex guides the tumor hierarchy's developmental trajectory.
  • Trithorax knockdown induced temporal reversion to an embryonic state, expanding CSCs.
  • Inactivation of Polycomb repressive complex 2 amplified tumor growth and CSC expansion.

Conclusions:

  • Inactivation of COMPASS and Polycomb complexes cooperates to disrupt tumor hierarchies.
  • This disruption leads to CSC plasticity, heterogeneity, and uncontrolled tumor expansion.
  • Understanding these interactions offers insights into cancer development and potential therapeutic targets.

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