Poster Presentation Epigenetics 2013

Repression of gene expression by the fission yeast SWI/SNF complex independent of its chromatin remodeling activity. (#106)

Brendon J Monahan 1 , Judit Villén 2 , Samual Marguerat 3 , Jürg Bähler 3 , Steve Gygi 2 , Fred Winston 2
  1. CSIRO, University of Melbourne, Parkville, VIC, Australia
  2. Harvard Medical School, Boston, MA, USA
  3. University College London, London, UK

The interaction of DNA with nucleosomal histones, the primary protein component of chromatin, can make DNA inaccessible to cellular factors required for DNA replication, recombination, repair, and transcription.  Factors such as the SWI/SNF ATP-dependent chromatin remodeling complexes modify chromatin structure to permit and regulate these fundamental processes.  The critical nature of SWI/SNF is illustrated by the fact that its inactivation in humans causes cancer and other diseases.  We have established the fission yeast, Schizosaccharomyces pombe, as a model system to study SWI/SNF function. There are two related but distinct chromatin remodeling complexes of the SWI/SNF class in cells, namely SWI/SNF and RSC (or BAF and pBAF in humans).  We have shown that the compositions of S. pombe SWI/SNF and RSC differ from their Saccharomyces cerevisiae counterparts and in some ways are more similar to the human complexes. Transcriptome analyses of various S. pombe SWI/SNF and RSC mutants have identified widespread requirements of these factors for transcription, including a role for SWI/SNF in the direct repression of iron uptake systems. Interestingly, this repressive role of SWI/SNF was independent of its chromatin remodeling activity, indicating that SWI/SNF mediates this repression via the recruitment of other chromatin factors such as histone deacetylases.