Two Subunits Specific to the PBAP Chromatin Remodeling Complex Have Distinct and Redundant Functions during Drosophila Development

Abstract

Chromatin remodeling complexes control the availability of DNA binding sites to transcriptional regulators. Two distinct conserved forms of the SWI/SNF class of complexes are characterized by the presence of specific accessory subunits. In Drosophila, the core Brahma complex associates either with Osa to form the BAP complex or with Bap170 and Bap180 to form the PBAP complex. osa mutations reproduce only a subset of the developmental phenotypes caused by mutations in subunits of the core complex. To test whether the PBAP complex performs the remaining functions, we generated mutations in bap170 and bap180. Surprisingly, we found that Bap180 is not essential for viability, although it is required in ovarian follicle cells for normal eggshell development. Bap170 is necessary to stabilize the Bap180 protein, but a mutant form that retains this function is sufficient for both survival and fertility. The two subunits act redundantly to allow metamorphosis; using gene expression profiling of bap170 bap180 double mutants, we found that the PBAP complex regulates genes involved in tissue remodeling and immune system function. Finally, we generated mutants lacking Bap170, Bap180, and Osa in the germ line to demonstrate that the core Brahma complex can function in oogenesis without any of these accessory subunits.

SUPPLEMENTAL MATERIAL

Supplemental material for this article may be found at http://mcb.asm.org/ .

ACKNOWLEDGMENTS

We thank Richard Carthew, Dominique Ferrandon, Bob Holmgren, Carl Thummel, the Developmental Studies Hybridoma Bank, the Gene Disruption Project, and the Bloomington Drosophila stock center for reagents and Jennifer Bandura and Vitor Barbosa for technical advice. We are grateful to the NYU Cancer Institute Genomics Facility for assistance with the microarray and quantitative RT-PCR experiments, and we thank Jinhua Wang for sequence analysis of genomic regions flanking genes regulated in the microarray. The manuscript was improved by the critical comments of Sergio Astigarraga, Kerstin Hofmeyer, Kevin Legent, Jean-Yves Roignant, and Josie Steinhauer.

This work was supported by the National Institutes of Health (grant GM56131 to J.E.T.).