The Drosophila ovary is a valuable model for the investigation of niche-stem cell interactions. In this model, BMP (Dpp) signals from the niche cap cells inhibit differentiation of germline stem cells (GSCs), at least partially through repression of the transcription factor bam. Away from the niche, germline cells are in contact with somatic escort cells, which support GSC differentiation and do not express dpp. Several mechanisms have been uncovered that contribute to the regulation of dpp expression and signal transduction, and on p. 3449, Rongwen Xi and co-workers reveal an important role for Polycomb group (PcG)-mediated modulation of dpp. Depletion of Polycomb repressive complex 1 (PRC1) components in escort cells causes aberrant expression of dpp, leading to tumour-like accumulation of GSCs and differentiation failure. This non-autonomous phenotype could be rescued by expression of bam in the GSCs. PcG usually acts in antagonism to Trithorax group (TrxG) complexes, and the authors further show that knockdown of the TrxG component brm reverses the PcG-depletion phenotype, so GSCs can once again differentiate. Unlike many other cases of PcG-TrxG antagonism, however, brm knockdown or overexpression alone has no effect, suggesting that PcG-mediated dpp repression may be the default state in escort cells. This work adds to our understanding of the mechanisms underlying niche-stem cell interactions and GSC differentiation, and underlines the importance of dynamic chromatin regulation.
