The genomic silencing of position-effect variegation in <i>Drosophila melanogaster</i>: interaction between the heterochromatin-associated proteins Su(var)3-7 and HP1

Delattre, Marion; Spierer, Anne; Tonka, Chia-Hwa; Spierer, Pierre

doi:10.1242/jcs.113.23.4253

Cited by 71 publications

(6 citation statements)

References 44 publications

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“…The Drosophila SU(VAR)3–7 heterochromatin protein has been shown to interact with HP1 (Delattre et al ., 2000). SU(VAR)3–9 bait constructs and SU(VAR)3–7 prey constructs were tested for interaction.…”

Section: Resultsmentioning

confidence: 99%

“…The bait constructs 1–188 and 81–188 were prepared by a Sal I self‐ligation of clones 1–569 and 81–635, respectively. HP1 and SU(VAR)3–7 bait and target constructs are described in Delattre et al . (2000), and were kindly provided by P.Spierer.…”

Section: Methodsmentioning

confidence: 99%

“…Su(var)2–5 encodes the heterochromatin protein HP1 (James and Elgin, 1986; Eissenberg et al ., 1990), which interacts with several other chromatin proteins and therefore might function as a linker module in heterochromatin protein complexes (Wang et al ., 2000). Su(var)3–7 encodes a protein that contains seven widely spaced zinc fingers, interacts with HP1 and has the potential to bind DNA (Cleard et al ., 1997; Delattre et al ., 2000). Association of SU(VAR)3–9 with heterochromatic regions in Drosophila was recently demonstrated (Schotta and Reuter, 2000).…”

Section: Introductionmentioning

confidence: 99%

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Central role of Drosophila SU(VAR)3-9 in histone H3-K9 methylation and heterochromatic gene silencing

2002

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Su(var)3±9 is a dominant modi®er of heterochromatin-induced gene silencing. Like its mammalian and Schizosaccharomyces pombe homologues, Su(var) 3±9 encodes a histone methyltransferase (HMTase), which selectively methylates histone H3 at lysine 9 (H3-K9). In Su(var)3±9 null mutants, H3-K9 methylation at chromocentre heterochromatin is strongly reduced, indicating that SU(VAR)3±9 is the major heterochromatin-speci®c HMTase in Drosophila. SU (VAR)3±9 interacts with the heterochromatin-associated HP1 protein and with another silencing factor, SU(VAR)3±7. Notably, SU(VAR)3±9±HP1 interaction is interdependent and governs distinct localization patterns of both proteins. In Su(var)3±9 null mutants, concentration of HP1 at the chromocentre is nearly lost without affecting HP1 accumulation at the fourth chromosome. By contrast, in HP1 null mutants SU(VAR)3±9 is no longer restricted at heterochromatin but broadly dispersed across the chromosomes. Despite this interdependence, Su(var)3±9 dominates the PEV modi®er effects of HP1 and Su(var)3±7 and is also epistatic to the Y chromosome effect on PEV. Finally, the human SUV39H1 gene is able to partially rescue Su(var)3±9 silencing defects. Together, these data indicate a central role for the SU(VAR)3±9 HMTase in heterochromatin-induced gene silencing in Drosophila.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Central role of Drosophila SU(VAR)3-9 in histone H3-K9 methylation and heterochromatic gene silencing

2002

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“…HP1a is also modestly enriched along the male X [ 124 , 125 , 126 ]. The morphology of the polytene male X chromosome is similarly affected by reduction of Su(var)3-9 and by reduction or overexpression of Su(var)3-7, a heterochromatin protein that interacts with HP1a and Su(var)3-9 [ 107 , 108 , 127 ]. The bloated X phenotype of Su(var)3-7 or Su(var)3-9 mutants is rescued by mutations in MSL complex members, revealing a genetic interaction with dosage compensation [ 107 ].…”

Section: Heterochromatin and The Male X Chromosomementioning

confidence: 99%

When Down Is Up: Heterochromatin, Nuclear Organization and X Upregulation

Makki

Meller

2021

Cells

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Organisms with highly differentiated sex chromosomes face an imbalance in X-linked gene dosage. Male Drosophila solve this problem by increasing expression from virtually every gene on their single X chromosome, a process known as dosage compensation. This involves a ribonucleoprotein complex that is recruited to active, X-linked genes to remodel chromatin and increase expression. Interestingly, the male X chromosome is also enriched for several proteins associated with heterochromatin. Furthermore, the polytenized male X is selectively disrupted by the loss of factors involved in repression, silencing, heterochromatin formation or chromatin remodeling. Mutations in many of these factors preferentially reduce male survival or enhance the lethality of mutations that prevent normal recognition of the X chromosome. The involvement of primarily repressive factors in a process that elevates expression has long been puzzling. Interestingly, recent work suggests that the siRNA pathway, often associated with heterochromatin formation and repression, also helps the dosage compensation machinery identify the X chromosome. In light of this finding, we revisit the evidence that links nuclear organization and heterochromatin to regulation of the male X chromosome.

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“…All members contain two conserved domains: the chromodomain and the chromo shadow domain, the latter being involved in interaction with protein partners (Aasland and Stewart, 1995; Koonin et al ., 1995). In Drosophila , we have shown that HP1 interacts with another heterochromatin‐associated modifier of variegation, Su(var)3‐7 (Cléard et al ., 1997; Delattre et al ., 2000). Drosophila HP1 also interacts with origin recognition complex (ORC) proteins and co‐localizes with the Arp4 protein in pericentric heterochromatin (Frankel et al ., 1997; Pak et al ., 1997).…”

Section: Introductionmentioning

confidence: 99%

Ectopic HP1 promotes chromosome loops and variegated silencing in Drosophila

et al. 2001

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A transgene inserted in euchromatin exhibits mosaic expression when targeted by a fusion protein made of the DNA-binding domain of GAL4 and the heterochromatin-associated protein HP1. The silencing responds to the loss of a dose of the dominant modi®ers of position-effect variegation Su(var)3-7 and Su(var)2-5, the locus encoding HP1. The genomic environs of the insertion site at 87C1 comprise the dispersed repetitive elements micropia and ag. In the presence of the GAL4±HP1 chimera, the polytene chromosomes of this line form loops between the insertion site of the transgene and six other sections of chromosome 3R, as well as, rarely, with pericentric and telomeric heterochromatin. In contrast to the insertion site of the transgene at 87C, the six loopforming sites in the euchromatic arm were each previously described as intercalary heterochromatin. Moreover, GAL4±HP1 tethering on one homologue trans-inactivates the reporter on the other. HP1, probably together with other partners, could thus facilitate the coalescence of dispersed middle repetitive sequences, and organize the heterochromatic structure responsible for the variegated silencing of nearby euchromatic genes.

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The genomic silencing of position-effect variegation in Drosophila melanogaster: interaction between the heterochromatin-associated proteins Su(var)3-7 and HP1

Cited by 71 publications

References 44 publications

Central role of Drosophila SU(VAR)3-9 in histone H3-K9 methylation and heterochromatic gene silencing

Central role of Drosophila SU(VAR)3-9 in histone H3-K9 methylation and heterochromatic gene silencing

When Down Is Up: Heterochromatin, Nuclear Organization and X Upregulation

Ectopic HP1 promotes chromosome loops and variegated silencing in Drosophila

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