Polycomb group mutants exhibit mitotic defects in syncytial cell cycles of Drosophila embryos

• Published in: Developmental biology 2006-02, Vol.290 (2), p.312-322
• Main Authors: O'Dor, Ester, Beck, Samantha A., Brock, Hugh W.
• Format: Article
• Language: English
• Subjects: Alleles; Animals; Cell Cycle; Cell Nucleus - metabolism; Chromatin - metabolism; Chromatin bridges; DNA - metabolism; Drosophila - embryology; Drosophila Proteins - metabolism; Embryo, Nonmammalian - metabolism; Female; Gene Expression Regulation, Developmental; Giant Cells - cytology; Heterozygote; Image Processing, Computer-Assisted; Microscopy, Confocal; Mitosis; Mitotic delay; Mutation; Nuclear fallout; Nuclear Proteins - metabolism; Phenotype; Polycomb; Polycomb Repressive Complex 2; Repressor Proteins - metabolism
• ISSN: 0012-1606; 1095-564X
• DOI: 10.1016/j.ydbio.2005.11.015

The Polycomb Group (PcG) of epigenetic regulators maintains the repressed state of Hox genes during development of Drosophila, thereby maintaining the correct patterning of the anteroposterior axis. PcG-mediated inheritance of gene expression patterns must be stable to mitosis to ensure faithful transmission of repressed Hox states during cell division. Previously, two PcG mutants, polyhomeotic and Enhancer of zeste, were shown to exhibit mitotic segregation defects in embryos, and condensation defects in imaginal discs, respectively. We show that polyhomeotic proximal but not polyhomeotic distal is necessary for mitosis. To test if other PcG genes have roles in mitosis, we examined embryos derived from heterozygous PcG mutant females for mitotic defects. Severe defects in sister chromatid segregation and nuclear fallout, but not condensation are exhibited by Polycomb, Posterior sex combs and Additional sex combs. By contrast, mutations in Enhancer of zeste (which encodes the histone methyltransferase subunit of the Polycomb Repressive Complex 2) exhibit condensation but not segregation defects. We propose that these mitotic defects in PcG mutants delay cell cycle progression. We discuss possible mitotic roles for PcG proteins, and suggest that delays in cell cycle progression might lead to failure of maintenance.