title: Mutations in ash1 and trx enhance P-element-dependent silencing in Drosophila melanogaster.
abstract: In Drosophila melanogaster, the mini-w(+) transgene in Pci is normally expressed throughout the adult eye; however, when other P or KP elements are present, a variegated-eye phenotype results, indicating random w(+) silencing during development called P-element-dependent silencing (PDS). Mutant Su(var)205 and Su(var)3-7 alleles act as haplo-suppressors/triplo-enhancers of this variegated phenotype, indicating that these heterochromatic modifiers act dose dependently in PDS. Previously, we recovered a spontaneous mutation of P{lacW}ci(Dplac) called P{lacW}ci(DplacE1) (E1) that variegated in the absence of P elements, presumably due to the insertion of an adjacent gypsy element. From a screen for genetic modifiers of E1 variegation, we describe here the isolation of five mutations in ash1 and three in trx that enhance the E1 variegated phenotype in a dose-dependent and cumulative manner. These mutant alleles enhance PDS at E1, and in E1/P{lacW}ci(Dplac), but suppress position effect variegation (PEV) at In(1)w(m)(4). This opposite action is consistent with a model where ASH1 and TRX mark transcriptionally active chromatin domains. If ASH1 or TRX function is lost or reduced, heterochromatin can spread into these domains creating a sink that diverts heterochromatic proteins from other variegating locations, which then may express a suppressed phenotype.
authors.affiliation: Department of Biological Sciences, CW 405, Biological Sciences Building, University of Alberta, Edmonton, AB T6G 2E9, Canada.|Department of Biological Sciences, CW 405, Biological Sciences Building, University of Alberta, Edmonton, AB T6G 2E9, Canada.
authors.forename: Allen
authors.initials: A
authors.lastname: McCracken
authors.affiliation: Department of Biological Sciences, CW 405, Biological Sciences Building, University of Alberta, Edmonton, AB T6G 2E9, Canada.|Department of Biological Sciences, CW 405, Biological Sciences Building, University of Alberta, Edmonton, AB T6G 2E9, Canada.
authors.forename: John
authors.initials: J
authors.lastname: Locke
mesh_terms: D000483:Alleles; D000818:Animals; D000090266:Chromobox Protein Homolog 5; D004268:DNA-Binding Proteins / Q000235:genetics*; D029721:Drosophila Proteins / Q000235:genetics*; D004331:Drosophila melanogaster / Q000235:genetics* / Q000502:physiology; D005260:Female; D020868:Gene Silencing; D056426:Genetic Loci; D006570:Heterochromatin / Q000235:genetics; D008297:Male; D009154:Mutation; D010641:Phenotype; D017422:Sequence Analysis, DNA; D013489:Suppression, Genetic; D014157:Transcription Factors / Q000235:genetics*; D019076:Transgenes
chemical_list: C490910:ASH1 protein, Drosophila; D004268:DNA-Binding Proteins; D029721:Drosophila Proteins; D006570:Heterochromatin; C000716867:Su(var)205 protein, Drosophila; D014157:Transcription Factors; D000090266:Chromobox Protein Homolog 5
keywords: Drosophila; chromatin; chromatine; expression génique; gene expression; heterochromatin; hétérochromatine; transgene; transgène