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PWWP-mutants of the transcriptional cofactor JASPer divert promoter and enhancer activities and suppress position effect variegation in Drosophila [Hi-C]

ABSTRACT: Su(var) genes control heterochromatin establishment and maintenance in Drosophila melanogaster. Through a new Su(var) screen, we identified Su140 and Su113 as very strong Su(var) mutants that are epistatic over Su(var)3-9 in the In(1)wm4h PEV rearrangement. Both Su140 and Su113 encode point mutations in the PWWP domain of the transcriptional cofactor JASPer that has described functions in protecting gene activity in euchromatin. In JasperSu140/Su140 and JasperSu113/Su113 nuclear cycle (NC14) mutant embryos, heterochromatic marks (H3K9me2 and H3K9me3) are reduced, while activating histone modifications (H3K4me1 and H3K27ac) become enriched at heterochromatin. Whereas epitope-tagged wild-type JASPer accumulates over H3K36me3-positive regions in gene bodies, mutant JASPerSu140 is redistributed to cis-regulatory motifs (CRM) in promoters and enhancers. At genes, JASPerSu140 relocates to transcriptional start sites (TSS). Also, one third of developmentally regulated enhancers, including the white enhancer, show enrichment for JASPerSu140 and display elevated levels of eRNA in JasperSu140/Su140 NC14 embryos. In addition, JasperSu140/Su140 mutants induce a partial decompaction of the heterochromatin compartment containing the In(1)wm4h rearrangement and activate satellite repeat expression. Together, these data define Jasper mutants as novel Su(var) genes and highlight the importance of maintaining the balance between euchromatic and heterochromatic domains for controlling position effect variegation.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE310813 | GEO | 2026/03/26

REPOSITORIES: GEO

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PWWP-mutants of the transcriptional cofactor JASPer divert promoter and enhancer activities and suppress position effect variegation in Drosophila

Project description:Su(var) genes control heterochromatin establishment and maintenance in Drosophila melanogaster. Through a new Su(var) screen, we identified Su140 and Su113 as very strong Su(var) mutants that are epistatic over Su(var)3-9 in the In(1)wm4h PEV rearrangement. Both Su140 and Su113 encode point mutations in the PWWP domain of the transcriptional cofactor JASPer that has described functions in protecting gene activity in euchromatin. In JasperSu140/Su140 and JasperSu113/Su113 nuclear cycle (NC14) mutant embryos, heterochromatic marks (H3K9me2 and H3K9me3) are reduced, while activating histone modifications (H3K4me1 and H3K27ac) become enriched at heterochromatin. Whereas wild-type JASPer is enriched over H3K36me3-positive regions in gene bodies, JASPerSu140 is redistributed to regulatory elements in promoters and enhancers. JASPerSu140 directly binds and activates the white gene enhancer in NC14 embryos and JasperSu140/Su140 mutants induce a partial decompaction of the heterochromatin compartment containing the In(1)wm4h rearrangement. In addition, JasperSu140/Su140 and JasperSu113/su113 mutants also display elevated levels for 359bp (satellite) repeat transcripts at later stages of development. Together, these data define Jasper mutants as novel Su(var) genes and highlight the importance of maintaining the balance between euchromatic and heterochromatic domains for controlling position effect variegation.

2026-03-26 | GSE310920 | GEO

PWWP-mutants of the transcriptional cofactor JASPer divert promoter and enhancer activities and suppress position effect variegation in Drosophila [ChIP-Seq]

Project description:Su(var) genes control heterochromatin establishment and maintenance in Drosophila melanogaster. Through a new Su(var) screen, we identified Su140 and Su113 as very strong Su(var) mutants that are epistatic over Su(var)3-9 in the In(1)wm4h PEV rearrangement. Both Su140 and Su113 encode point mutations in the PWWP domain of the transcriptional cofactor JASPer that has described functions in protecting gene activity in euchromatin. In JasperSu140/Su140 and JasperSu113/Su113 nuclear cycle (NC14) mutant embryos, heterochromatic marks (H3K9me2 and H3K9me3) are reduced, while activating histone modifications (H3K4me1 and H3K27ac) become enriched at heterochromatin. Whereas epitope-tagged wild-type JASPer accumulates over H3K36me3-positive regions in gene bodies, mutant JASPerSu140 is redistributed to cis-regulatory motifs (CRM) in promoters and enhancers. At genes, JASPerSu140 relocates to transcriptional start sites (TSS). Also, one third of developmentally regulated enhancers, including the white enhancer, show enrichment for JASPerSu140 and display elevated levels of eRNA in JasperSu140/Su140 NC14 embryos. In addition, JasperSu140/Su140 mutants induce a partial decompaction of the heterochromatin compartment containing the In(1)wm4h rearrangement and activate satellite repeat expression. Together, these data define Jasper mutants as novel Su(var) genes and highlight the importance of maintaining the balance between euchromatic and heterochromatic domains for controlling position effect variegation.

2026-03-26 | GSE310811 | GEO

PWWP-mutants of the transcriptional cofactor JASPer divert promoter and enhancer activities and suppress position effect variegation in Drosophila [Cut & Tag]

Project description:Su(var) genes control heterochromatin establishment and maintenance in Drosophila melanogaster. Through a new Su(var) screen, we identified Su140 and Su113 as very strong Su(var) mutants that are epistatic over Su(var)3-9 in the In(1)wm4h PEV rearrangement. Both Su140 and Su113 encode point mutations in the PWWP domain of the transcriptional cofactor JASPer that has described functions in protecting gene activity in euchromatin. In JasperSu140/Su140 and JasperSu113/Su113 nuclear cycle (NC14) mutant embryos, heterochromatic marks (H3K9me2 and H3K9me3) are reduced, while activating histone modifications (H3K4me1 and H3K27ac) become enriched at heterochromatin. Whereas epitope-tagged wild-type JASPer accumulates over H3K36me3-positive regions in gene bodies, mutant JASPerSu140 is redistributed to cis-regulatory motifs (CRM) in promoters and enhancers. At genes, JASPerSu140 relocates to transcriptional start sites (TSS). Also, one third of developmentally regulated enhancers, including the white enhancer, show enrichment for JASPerSu140 and display elevated levels of eRNA in JasperSu140/Su140 NC14 embryos. In addition, JasperSu140/Su140 mutants induce a partial decompaction of the heterochromatin compartment containing the In(1)wm4h rearrangement and activate satellite repeat expression. Together, these data define Jasper mutants as novel Su(var) genes and highlight the importance of maintaining the balance between euchromatic and heterochromatic domains for controlling position effect variegation.

2026-03-26 | GSE310810 | GEO

HP1a, Su(var)3-9, SETDB1 and POF stimulate or repress gene expression depending on genomic position, gene length and expression pattern in Drosophila melanogaster

Project description:Heterochromatin protein 1a (HP1a) is a chromatin associated protein that has been well studied in many model organisms, such as Drosophila, where it is a determining factor for classical heterochromatin. HP1a is associated with the two histone methyltransferases SETDB1 and Su(var)3-9, which mediate H3K9 methylation marks and participate in the establishment and spreading of HP1a enriched chromatin. While HP1a is generally regarded as a factor that represses gene transcription, several reports have linked HP1a binding to active genes, and in some cases, it has been shown to stimulate transcriptional activity. To clarify the function of HP1a in transcription regulation and its association with Su(var)3-9, SETDB1 and the chromosome 4 specific protein POF, we conducted genome-wide expression studies and combined the results with available binding data in Drosophila melanogaster. The results suggested that HP1a has a repressing function on chromosome 4, where it preferentially targets non-ubiquitously expressed genes (NUEGs), and a stimulating function in pericentromeric regions. Further, we showed that the effects of SETDB1 and Su(var)3-9 are similar to HP1a, and on chromosome 4, Su(var)3-9, SETDB1 and HP1a target the same genes. In contrast, transposons are repressed by HP1a and Su(var)3-9 but are un-affected by SETDB1 and POF. In addition, we found that the binding level and expression effects of HP1a are affected by gene length. Our results indicate that genes have adapted to be properly expressed in their local chromatin environment. We prepared total RNA from 1st instar larvae trans-heterozygous for HP1a04/HP1a05, trans-heterozygous Su(var)3-9evo/Su(var)3-906, homozygous Setdb110.1/ Setdb110.1 mutants and trans-heterozygous HP1a04 PofD119/HP1a05 PofD119 double mutants three biological replicates, as well as from six biological replicates of wildtype control 1st instar larvae.

2013-04-05 | E-GEOD-43478 | biostudies-arrayexpress

High-resolution mapping of HP1 redistribution in a position-effect variegation model

Project description:Position-effect variegation (PEV) is the stochastic transcriptional silencing of a gene positioned adjacent to heterochromatin. white-mottled X-chromosomal inversions in Drosophila are classic PEV models that show variegation of the eye color gene white due to its relocation next to pericentric heterochromatin. To obtain insight into the mechanism of PEV, we constructed detailed binding maps of Heterochromatin Protein 1 (HP1), a major component of heterochromatin, on white-mottled chromosomes. We find that HP1 invades euchromatin across the inversion breakpoints over ~175kb and ~30kb, causing de novo association of HP1 with 20 genes. However, HP1 binding levels in these regions show substantial local variation; white is most strongly bound by HP1 and is one of only two genes that are substantially repressed by heterochromatin. HP1 binding to the invaded region is exceptionally sensitive to the dosage of the histone methyltransferase Su(var)3-9, indicating that the de novo formed heterochromatin is relatively unstable. Our molecular maps demonstrate that heterochromatin can invade a normally euchromatic region, yet the strength of HP1 binding and effects on gene expression are highly dependent on local context. Keywords: DamID, gene expression, genetic modification.

2009-02-18 | GSE12395 | GEO

Binding of SU(VAR)3-9 partially depends on SETDB1 in the chromosomes of Drosophila melanogaster

Project description:Histone modifications are a class of epigenetic marks with prominent roles in gene regulation in eukaryotes. One such mark, predominantly inactivation-related, is methylation of histone H3 lysine 9 (H3K9). In the present study, we decipher the interplay between two evolutionary conserved Drosophila H3K9-specific histone methyltransferases, SU(VAR)3-9 and SETDB1. We asked whether SETDB1 is required for targeting of SU(VAR)3-9. Using DamID-seq, we obtained SU(VAR)3-9 binding profiles for the chromosomes from larval salivary glands and germline cells from adult females, and compared profiles between the wild type and SETDB1-mutant backgrounds. Our analyses indicate that the vast majority of single-copy genes in euchromatin are targeted by SU(VAR)3-9 only in the presence of SETDB1, whereas repeated sequences in heterochromatin is largely SETDB1-independent. Interestingly, piRNA clusters 42AB and 38C behave differently in terms of SU(VAR)3-9 binding in somatic and germline cells. Namely, SU(VAR)3-9 binding to these piRNA clusters is independent of SETDB1 in somatic cells, whereas it is SETDB1-dependent in the germline. In addition, we compared SU(VAR)3-9 profiles in female germline cells at different developmental stages (whole juvenile ovaries and mature nurse cells). It turned out that SU(VAR)3-9 binding is influenced both by the presence of SETDB1, as well as by the differentiation stage.

2019-07-16 | GSE134250 | GEO

JASPer controls interphase histone H3S10 phosphorylation by chromosomal kinase JIL-1 in Drosophila

Project description:In Drosophila the chromosomal kinase JIL-1 is responsible for most interphase histone H3S10 phosphorylation and has been proposed to protect active chromatin from acquiring heterochromatic marks, like dimethylated histone H3K9 (H3K9me2) and HP1. Here, we show that JIL-1’s targeting to chromatin depends on a PWWP domain-containing protein JASPer (JIL-1 Anchoring and Stabilizing Protein). The JASPer-JIL-1 (JJ)-complex is the major form of the kinase in vivo and is targeted to active genes and telomeric transposons via binding of the PWWP domain of JASPer to H3K36me3 nucleosomes, where the complex modulates the transcriptional output. JIL-1 and JJ-complex depletion in cycling cells lead to small changes in H3K9me2 distribution at active genes and telomeric transposons. Finally, we identify several interactors of the endogenous JJ-complex and propose that JIL-1 not only prevents heterochromatin formation but also coordinates chromatin-based regulation in the transcribed part of the genome.

2019-10-09 | PXD012790 | Pride

Loss of Su(var)3-9 and SetDB1 disrupts late stages of larval development of Drosophila

Project description:Methylation of H3K9 histone residue is a marker of gene silencing in eukaryotes. Three enzymes responsible for adding this modification – G9a, SetDB1/Egg, and Su(var)3-9 – are known in Drosophila. To understand how simultaneous mutations of SetDB1 and Su(var)3-9, or all three proteins may affect the fly development, appropriate combinations were obtained. Double mutants egg; Su(var)3-9 displayed pronounced embryonic lethality, slower larval growth and died before or during metamorphosis. Analysis of transcription in larval salivary glands and wing imaginal disks indicated that the effect of double mutation is tissue-specific. In salivary gland chromosomes, affected genes display low H3K9me2 enrichment and are rarely bound by SetDB1 or Su(var)3-9. We suppose that each of these enzymes directly or indirectly controls its own set of gene targets in different organs, and double mutation results in an imbalanced developmental program. This also indicates that SetDB1 and Su(var)3-9 may affect transcription via H3K9-independent mechanisms. Unexpectedly, in double and triple mutants, amount of di-and tri-methylated H3K9 is drastically reduced, but not completely absent. We hypothesize that this residual methylation implies the existence of additional H3K9-specific methyltransferase in Drosophila.

2023-12-25 | GSE223579 | GEO

HP1a recruitment to promoters is independent of H3K9 methylation in Drosophila melanogaster

Project description:Heterochromatin protein 1 (HP1) proteins are important regulators of heterochromatin mediated gene silencing and chromosome structure and it is well known as the reader of the heterochromatin mark methylation of histone H3 lysine 9 (H3K9me). In Drosophila three different histone lysine methyl transferases (HKMTs) are associated with the methylation of H3K9; Su(var)3-9, Setdb1 and G9a. To gain insights on the dependence of HP1a on the three different HKMTs, the division of labor between these methyl transferases and the dependence of HP1a on H3K9me we have studied HP1a binding in relation to H3K9me in mutants of these HKMTs. We show that Su(var)3-9 is responsible for the HP1a H3K9me-dependent binding in pericentromeric regions while Setdb1 controls the HP1a H3K9me-dependent binding to cytological region 2L:31 and together with POF chromosome 4. HP1a binds to the promoters and within gene bodies of active genes in these three regions. More importantly, HP1a bound at promoters of active genes are independent of H3K9me and POF and is associated to heterochromatin protein 2 (HP2) and open chromatin. Our results supports a model where HP1a nucleates with high affinity independent of H3K9me in promoters of active genes and then spreads via H3K9 methylation and transient looping contacts with those H3K9me target sites. In total 44 samples; 2 replicates for each genotype and for each ChIP (HP1a, H3K9me2 and H3K9me3)

2012-12-21 | E-GEOD-38366 | biostudies-arrayexpress

HP1a, Su(var)3-9, SETDB1 and POF stimulate or repress gene expression depending on genomic position, gene length and expression pattern in Drosophila melanogaster

2013-04-05 | GSE43478 | GEO