Multiple SET Methyltransferases Are Required to Maintain Normal Heterochromatin Domains in the Genome of Drosophila melanogaster
Open accessAbstract
Methylation of histone H3 lysine 9 (H3K9) is a key feature of silent chromatin and plays an important role in stabilizing the interaction of heterochromatin protein 1 (HP1) with chromatin. Genomes of metazoans such as the fruit fly Drosophila melanogaster generally encode three types of H3K9-specific SET domain methyltransferases that contribute to chromatin homeostasis during the life cycle of the organism. SU(VAR)3-9, dG9a, and dSETDB1 all function in the generation of wild-type H3K9 methylation levels in the Drosophila genome. Two of these enzymes, dSETDB1 and SU(VAR)3-9, govern heterochromatin formation in distinct but overlapping patterns across the genome. H3K9 methylation in the small, heterochromatic fourth chromosome of D. melanogaster is governed mainly by dSETDB1, whereas dSETDB1 and SU(VAR)3-9 function in concert to methylate H3K9 in the pericentric heterochromatin of all chromosomes, with dG9a having little impact in these domains, as shown by monitoring position effect variegation. To understand how these distinct heterochromatin compartments may be differentiated, we examined the developmental timing of dSETDB1 function using a knockdown strategy. dSETDB1 acts to maintain heterochromatin during metamorphosis, at a later stage in development than the reported action of SU(VAR)3-9. Surprisingly, depletion of both of these enzymes has less deleterious effect than depletion of one. These results imply that dSETDB1 acts as a heterochromatin maintenance factor that may be required for the persistence of earlier developmental events normally governed by SU(VAR)3-9. In addition, the genetic interactions between dSETDB1 and Su(var)3-9 mutations emphasize the importance of maintaining the activities of these histone methyltransferases in balance for normal genome function.
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Germline knockdown of Su(var)3-9 leads to much more severe oogenesis defects than Egg depletion but also induces a 2-3-fold upregulation of R1 and R2 elements.
“GKD of another HMT, Su(var)3–9 known to be involved in the formation of constitutive heterochromatin and the spreading of the H3K9me3 mark (84–86) led to much more severe defects of oogenesis than Egg depletion but also induced a 2–3-fold upregulation of R1 and R2 elements (Figure 2A).”
From Impaired function of rDNA transcription initiation machinery leads to derepression of ribosomal genes with insertions of R2 retrotransposon (2022) · cites this paper as [85]
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- Authors
- Brower-Toland, B., Riddle, N. C., Jiang, H., Huisinga, K. L., & Elgin, S. C. R.
- Affiliations
- Department of Biology , Washington University, St. Louis, Missouri 63130 and
- Washington University in St. Louis (US)
- Northwestern University (US)
- Corresponding author
- Elgin, Sarah C R
- Venue
- Genetics
- Publisher
- Oxford University Press (OUP)
- Published
- 2009-04-01
- Volume
- 181
- Issue
- 4
- Pages
- 1303-1319
- ISSN
- 0016-6731 (ISSN-L)
- 1943-2631
- PMC
- PMC2666501
- OpenAlex
- W2171405275
- Cited by
- 86
- References
- 45
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 4 · 2023: 4 · 2022: 3 · 2021: 5 · 2020: 4 · 2019: 9 · 2018: 6 · 2017: 3 · 2016: 6 · 2015: 7 · 2014: 6 · 2013: 7 · 2012: 5
- FWCI
- 2.55
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model (vor)
- Locations
- Genetics (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of General Medical Sciences (R01 GM68388, F32GM078833, R01GM068388)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Agricultural and Biological Sciences › Plant Science › Chromosomal and Genetic Variations
- Keywords
- H3K9 methylation, heterochromatin, Drosophila melanogaster, Su(var)3-9, HP1, position effect variegation, pericentromeric heterochromatin, chromosome 4, metamorphosis, developmental timing, genetic interactions
- MeSH terms
- Animals, Drosophila melanogaster, Epistasis, Genetic, Heterochromatin, Larva, Models, Biological, Phenotype, Histone-Lysine N-Methyltransferase, Repressor Proteins, Mutagenesis, Gene Expression Regulation, Developmental, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling, Drosophila Proteins, Animals, Genetically Modified, Chromatin Assembly and Disassembly, Genome, Insect, Mutant Proteins
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