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Histone locus regulation by the Drosophila dosage compensation adaptor protein CLAMP

ABSTRACT: The conserved histone locus body (HLB) assembles prior to zygotic gene activation early during development and concentrates factors into a nuclear domain of coordinated histone gene regulation. Although HLBs form specifically at replication-dependent histone loci, the cis and trans factors that target HLB components to histone genes remained unknown. Here we report that conserved GA repeat cis elements within the bidirectional histone3-histone4 promoter direct HLB formation in Drosophila In addition, the CLAMP (chromatin-linked adaptor for male-specific lethal [MSL] proteins) zinc finger protein binds these GA repeat motifs, increases chromatin accessibility, enhances histone gene transcription, and promotes HLB formation. We demonstrated previously that CLAMP also promotes the formation of another domain of coordinated gene regulation: the dosage-compensated male X chromosome. Therefore, CLAMP binding to GA repeat motifs promotes the formation of two distinct domains of coordinated gene activation located at different places in the genome.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE119448 | GEO | 2018/09/05

REPOSITORIES: GEO

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Histone locus regulation by the Drosophila dosage compensation adaptor protein CLAMP

Project description:The conserved histone locus body (HLB) assembles prior to zygotic gene activation early during development and concentrates factors into a nuclear domain of coordinated histone gene regulation. Although HLBs form specifically at replication dependent histone loci, the cis and trans factors that target HLB components to histone genes remained unknown. Here we report that conserved GA-repeat cis elements within the bidirectional histone3-histone4 promoter direct HLB formation in Drosophila. In addition, the CLAMP zinc-finger protein binds these GA-repeat motifs, increases chromatin accessibility, enhances histone gene transcription, and promotes HLB formation. We previously demonstrated that CLAMP also promotes the formation of another domain of coordinated gene regulation: the dosage-compensated male X-chromosome. Therefore, CLAMP binding to GA-repeat motifs promotes the formation of two distinct domains of coordinated gene activation located at different places in the genome.

2017-11-15 | GSE102922 | GEO

Drosophila Histone Locus Body assembly and function involves multiple interactions

Project description:The histone locus body (HLB) assembles at replication-dependent (RD) histone loci and concentrates factors required for RD histone mRNA biosynthesis. The D. melanogaster genome has a single locus comprised of ~100 copies of a tandemly arrayed 5 kB repeat unit containing one copy of each of the 5 RD histone genes. To determine sequence elements required for D. melanogaster HLB formation and histone gene expression, we used transgenic gene arrays containing 12 copies of the histone repeat unit that functionally complement loss of the ~200 endogenous RD histone genes. A 12x histone gene array in which all H3-H4 promoters were replaced with H2a-H2b promoters (12xPR) does not form an HLB or express high levels of RD histone mRNA in the presence of the endogenous histone genes. In contrast, this same transgenic array is active in HLB assembly and RD histone gene expression in the absence of the endogenous RD histone genes and rescues the lethality caused by homozygous deletion of the RD histone locus. The HLB formed in the absence of endogenous RD histone genes on the mutant 12x array contains all known factors present in the wild type HLB including CLAMP, which normally binds to GAGA repeats in the H3-H4 promoter. These data suggest that multiple protein-protein and/or protein-DNA interactions contribute to HLB formation, and that the large number of endogenous RD histone gene copies sequester available factor(s) from attenuated transgenic arrays, thereby preventing HLB formation and gene expression. ChIP-qPCR and ChIP-Seq experiments were done on homozygous histone locus (HisC) deletion embryos rescued by the 12 copy promoter replacement (PR) or designer wild type (DWT) arrays on the third chromosome (VK33) to determine CLAMP's interaction with the locus

2020-05-12 | GSE150297 | GEO

CLAMP and Zelda function together as pioneer transcription factors to promote Drosophila zygotic genome activation [ChIP-Seq]

Project description:The pioneer transcription factor Zelda (ZLD) increases the accessibility of chromatin to promote the essential process of zygotic genome activation (ZGA) in the Drosophila early embryo. However, many genomic loci remain accessible in the absence of ZLD and are enriched for GA-rich DNA binding motifs. Therefore, we hypothesized that other pioneer TFs that function with ZLD have not yet been identified, especially those that bind to GA-rich motifs. CLAMP (Chromatin-linked adaptor for Male-specific lethal MSL proteins) is a GA-rich motif binding TF that is essential for early embryonic development. Here, we identify for the first time that CLAMP is a pioneer TF which interacts directly with nucleosomes, regulates zygotic genome activation, promotes chromatin accessibility, and facilitates the binding of ZLD to promoters. When ZLD is bound at a locus but does not regulate chromatin accessibility, CLAMP can often function redundantly to open the chromatin. Because ZGA is an essential process across metazoans, it is key to evolve redundant pioneer TFs to protect organisms from lethality that would be caused by loss of a single non-redundant factor.

2021-08-05 | GSE152598 | GEO

CLAMP and Zelda function together as pioneer transcription factors to promote Drosophila zygotic genome activation [ATAC-Seq]

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Identifying splicing targets of CLAMP by mRNA-sequencing

Project description:CLAMP is a GA-repeat motif binding transcription factor that regulates gene expression. We hypothesized that CLAMP also regulates RNA processing, specifically alternative splicing that occurs co-transcriptionally because CLAMP is bound to intronic regions that are rich in polypyrimidine tracts which contain GA-rich sequences. Furthermore, GA-rich repeat sequences are thought to have evolved from polypyrimidine tracts that regulate splicing. Also, MALDI-mass spectrometry data identifying putative CLAMP interactors found association with 33 RNA binding proteins, including 6 that regulate alternative splicing. Thus, to test our hypothesis that CLAMP shapes transcriptome diversity by regulating RNA transcript splicing, we performed mRNA-sequencing in the presence and absence of CLAMP in Kc (female) and S2 (male) cell lines and used a SUPPA based pipeline called time2splice (https://github.com/ashleymaeconard/time2splice) to analyze the sequencing data. Using both cell lines helped us to identify female (Kc) and male (S2) specific splicing events. We identified 452 genes differentially spliced beetween Kc and S2 cells. There are 46 and 113 CLAMP-dependent splicing events in Kc and S2 cells, respectively. Interestingly, 45 CLAMP-dependent events (belonging to 42 genes) are specific to Kc cells, i.e female-specific, whereas 112 CLAMP dependent events (belonging to 100 genes) in S2 cells are specific to S2 cells, i.e male-specific. Therefore, we identified a new role for the transcription factor CLAMP in regulated sex-specific splicing events in Kc and S2 cells.

2023-08-02 | GSE220439 | GEO

Factor cooperation for chromosome discrimination in Drosophila

Project description:Transcription regulators select their genomic binding sites from a large pool of similar, non‑functional sequences. Although general principles that allow such discrimination are known, the complexity of DNA elements often precludes a prediction of functional sites. The process of dosage compensation in Drosophila allows exploring the rules underlying binding site selectivity. The male-specific-lethal (MSL) Dosage Compensation Complex selectively binds to some 300 X-chromosomal ‘High Affinity Sites’ (HAS) containing GA‑rich ‘MSL recognition elements’ (MREs), but disregards thousands of other MRE sequences in the genome. The DNA‑binding subunit MSL2 alone identifies a subset of MREs, but fails to recognize most MREs within HAS. The ‘Chromatin-linked adaptor for MSL proteins’ (CLAMP) also interacts with many MREs genome‑wide and promotes DCC binding to HAS. Using genome‑wide DNA‑immunoprecipitation we describe extensive cooperativity between both factors, depending on the nature of the binding sites. These are explained by physical interaction between MSL2 and CLAMP. In vivo, both factors cooperate to compete with nucleosome formation at HAS. The male‑specific MSL2 thus synergises with a ubiquitous GA‑repeat binding protein for refined X/autosome discrimination.

2018-12-05 | GSE119708 | GEO

Long-range genomic contacts and spatiotemporal chromatin landscape of human histone gene clusters at Histone Locus Bodies during the cell cycle in breast cancer [cHiC]

Project description:Cell cycle controlled mechanistic remodeling of chromatin architecture at HLBs as non-membranous phase-separated nuclear domains represents a novel dimension to regulation of cell proliferation. Therefore, we sought to resolve a gap in our understanding of how 3D higher-order genomic organization supports the activation of multiple clustered histone genes. Our findings are consistent model that the HINFP/NPAT complex controls the formation and dynamic remodeling of higher-order genomic organization of histone gene clusters at HLBs in early to late G1 phase to support production of histone mRNAs in S phase. that the two principal histone gene regulators HINFP and NPAT are located at anchor-points for chromatin loops reflecting their obligatory functions in remodeling the spatiotemporal genomic organization at HLBs during the G1 phase to accommodate histone gene expression in S phase.

2023-05-10 | GSE229296 | GEO

Long-range genomic contacts and spatiotemporal chromatin landscape of human histone gene clusters at Histone Locus Bodies during the cell cycle in breast cancer [ChIP-seq]

2023-05-10 | GSE229295 | GEO

Enhanced chromatin accessibility of the dosage compensated Drosophila male X chromosome requires the CLAMP zinc finger protein [MNase-SEQ]

Project description:The essential process of dosage compensation is required to equalize gene expression of X-chromosome genes between males (XY) and females (XX). In Drosophila, the conserved Male-specific lethal (MSL) histone acetyltransferase complex mediates dosage compensation by increasing transcript levels from genes on the single male X-chromosome approximately two-fold. Consistent with its increased levels of transcription, the male X-chromosome has enhanced chromatin accessibility, distinguishing it from the autosomes. Here, we demonstrate that the non-sex specific CLAMP (Chromatin-linked adaptor for MSL proteins) zinc finger protein that recognizes GA-rich sequences genome-wide promotes the specialized chromatin environment on the male X-chromosome. In contrast, MSL complex is not required for global male X-chromosome chromatin accessibility, and instead promotes chromatin accessibility just at its highest-occupancy sites. Overall, our results support a model where synergy between the global increases in accessibility promoted by CLAMP and the local effects of MSL complex create a specialized chromatin domain on the male X-chromosome.

2017-10-31 | GSE99893 | GEO

Enhanced chromatin accessibility of the dosage compensated Drosophila male X chromosome requires the CLAMP zinc finger protein [START-SEQ]

2017-10-31 | GSE99842 | GEO

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