A Role for the Drosophila SU(VAR)3-9 Protein in Chromatin Organization at the Histone Gene Cluster and in Suppression of Position-Effect Variegation

• Published in: Genetics (Austin) Vol. 162; no. 4; pp. 1763 - 1774
• Main Authors: Ner, Sarbjit S, Harrington, Michael J, Grigliatti, Thomas A
• Format: Journal Article
• Language: English
• Published: United States Genetics Soc America 01-12-2002; Genetics Society of America
• Subjects: Animals; Base Sequence; Chromatin - genetics; Deoxyribonucleic acid; DNA; DNA - genetics; Drosophila - genetics; Drosophila - growth & development; Drosophila - metabolism; Drosophila Proteins - genetics; Female; Gene Expression Regulation, Developmental; Genes; Genes, Insect; Genetics; Histone Methyltransferases; Histone-Lysine N-Methyltransferase; Histones - genetics; Male; Methyltransferases - genetics; Multigene Family; Mutation; Protein Methyltransferases; Repressor Proteins - genetics; RNA, Messenger - genetics; RNA, Messenger - metabolism; Suppression, Genetic
• ISSN: 0016-6731; 1943-2631; 1943-2631
• DOI: 10.1093/genetics/162.4.1763

Mutations in the gene for Su(var)3-9 are dominant suppressors of position-effect variegation (PEV). We show that SU(VAR)3-9 is a chromatin-associated protein and identify the large multicopy histone gene cluster (HIS-C) as one of its target loci. The organization of nucleosomes over the entire HIS-C region is altered in Su(var)3-9 mutants and there is a concomitant increase in expression of the histone genes. SU(VAR)3-9 is a histone H3 methyltransferase and, using chromatin immunoprecipitation, we show that SU(VAR)3-9 is present at the HIS-C locus and that the histone H3 at the HIS-C locus is methylated. We propose that SU(VAR)3-9 is involved in packaging HIS-C into a distinct chromatin domain that has some of the characteristics of beta-heterochromatin. We suggest that methylation of histone H3 is important for the chromatin structure at HIS-C. The chromosomal deficiency for the HIS-C is also a suppressor of PEV. In contrast to what might be expected, we show that hemizygosity for the HIS-C locus leads to a substantial increase in the histone transcripts.