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Dose-dependent functions of SWI/SNF BAF in permitting and inhibiting cell proliferation in vivo

Aniek van der Vaart1, Molly Godfrey1, Vincent Portegijs1

  • 1Developmental Biology, Department of Biology, Faculty of Sciences, Utrecht University, Padualaan 8, 3584 CH Utrecht, Netherlands.

Science Advances
|June 5, 2020
PubMed

Insights

Switch/sucrose nonfermenting (SWI/SNF) complexes control cell division and differentiation. Incomplete SWI/SNF inactivation can halt tumor suppression while preserving essential gene regulation.

Area of Science:

  • Molecular Biology
  • Developmental Biology
  • Genetics

Background:

  • Switch/sucrose nonfermenting (SWI/SNF) complexes are crucial for transcription and chromatin remodeling.
  • Polycomb group (PcG) proteins mediate gene silencing, opposing SWI/SNF functions.
  • SWI/SNF gene mutations are common in human cancers, highlighting their role in development and disease.

Purpose of the Study:

  • To investigate the in vivo roles of SWI/SNF and PcG complexes in regulating cell proliferation and differentiation.
  • To understand how varying SWI/SNF BAF component levels impact cell fate decisions during development.

Main Methods:

  • Utilized the nematode *Caenorhabditis elegans* for its reproducible developmental processes.
  • Employed RNA interference (RNAi) and lineage-specific gene knockout to manipulate SWI/SNF components.
  • Applied targeted protein degradation techniques to control SWI/SNF BAF levels in vivo.

Main Results:

  • Altered SWI/SNF BAF levels led to either excessive cell proliferation or complete cell cycle arrest.
  • High SWI/SNF BAF dosage is required to halt cell division during differentiation and counteract PcG repression.
  • Low SWI/SNF protein levels promote cell proliferation and hyperplasia, even when PcG repression is inhibited.

Conclusions:

  • SWI/SNF BAF dosage critically determines cell proliferation versus differentiation.
  • Incomplete SWI/SNF inactivation can abolish tumor suppressor functions while retaining transcriptional regulation.
  • These findings offer insights into cancer development and the complex roles of chromatin remodelers.

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