title: The Trithorax-mimic allele of Enhancer of zeste renders active domains of target genes accessible to polycomb-group-dependent silencing in Drosophila melanogaster.
abstract: Two antagonistic groups of genes, the trithorax- and the Polycomb-group, are proposed to maintain the appropriate active or inactive state of homeotic genes set up earlier by transiently expressed segmentation genes. Although some details about the mechanism of maintenance are available, it is still unclear how the initially active or inactive chromatin domains are recognized by either the trithorax-group or the Polycomb-group proteins. We describe an unusual dominant allele of a Polycomb-group gene, Enhancer of zeste, which mimics the phenotype of loss-of-function mutations in trithorax-group genes. This mutation, named E(z)(Trithorax mimic) [E(z)(Trm)], contains a single-amino-acid substitution in the conserved SET domain. The strong dominant trithorax-like phenotypes elicited by this E(z) allele suggest that the mutated arginine-741 plays a critical role in distinguishing between active and inactive chromatin domains of the homeotic gene complexes. We have examined the modification of E(z)(Trm) phenotypes by mutant alleles of PcG and trxG genes and other mutations that alter the phosphorylation of nuclear proteins, covalent modifications of histones, or histone dosage. These data implicate some trxG genes in transcriptional repression as well as activation and provide genetic evidence for involvement of histone modifications in PcG/trxG-dependent transcriptional regulation.
authors.affiliation: Institute of Genetics, Biological Research Center, H-6701 Szeged, Hungary.
authors.forename: I
authors.initials: I
authors.lastname: Bajusz
authors.forename: L
authors.initials: L
authors.lastname: Sipos
authors.forename: Z
authors.initials: Z
authors.lastname: Györgypál
authors.forename: E A
authors.initials: EA
authors.lastname: Carrington
authors.forename: R S
authors.initials: RS
authors.lastname: Jones
authors.forename: J
authors.initials: J
authors.lastname: Gausz
authors.forename: H
authors.initials: H
authors.lastname: Gyurkovics
mesh_terms: D000107:Acetylation; D000483:Alleles; D000595:Amino Acid Sequence; D000818:Animals; D002087:Butyrates / Q000494:pharmacology; D002874:Chromosome Mapping; D002875:Chromosomes / Q000648:ultrastructure; D004268:DNA-Binding Proteins / Q000235:genetics*; D029721:Drosophila Proteins; D004331:Drosophila melanogaster / Q000235:genetics*; D020868:Gene Silencing; D005799:Genes, Dominant; D006579:Heterozygote; D006657:Histones / Q000378:metabolism; D007150:Immunohistochemistry; D019476:Insect Proteins / Q000235:genetics*; D008969:Molecular Sequence Data; D009154:Mutation; D009687:Nuclear Proteins / Q000235:genetics*; D010641:Phenotype; D063150:Polycomb Repressive Complex 1; D063151:Polycomb Repressive Complex 2; D011485:Protein Binding; D017434:Protein Structure, Tertiary; D012097:Repressor Proteins / Q000235:genetics*; D012469:Salivary Glands / Q000648:ultrastructure; D017422:Sequence Analysis, DNA; D014157:Transcription Factors; D014158:Transcription, Genetic
chemical_list: D002087:Butyrates; D004268:DNA-Binding Proteins; D029721:Drosophila Proteins; D006657:Histones; D019476:Insect Proteins; D009687:Nuclear Proteins; C066770:Pc protein, Drosophila; D012097:Repressor Proteins; D014157:Transcription Factors; C063460:Trl protein, Drosophila; C083329:E(z) protein, Drosophila; D063151:Polycomb Repressive Complex 2; D063150:Polycomb Repressive Complex 1