Factor cooperation for chromosome discrimination in<i>Drosophila</i>

Albig, Christian; Tikhonova, Evgeniya; Krause, Silke; Maksimenko, Oksana; Regnard, Catherine; Becker, Peter B.

doi:10.1093/nar/gky1238

Cited by 37 publications

(88 citation statements)

References 72 publications

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“…To characterize the direct DNA binding of MSL2, DNA fragments from paired-end sequencing runs were computationally subset to sizes between 10 and 130 bp, i.e., sub-nucleosomal length, since it has been previously shown that HAS are nucleosome-free [8,12]. For clarity, we refer to those binding events as direct "DNA" binding ( Fig 2A).…”

Section: Chromatin Binding Of Msl2 Precedes Complete Dosage Compensationmentioning

confidence: 99%

“…Antibodies aMSL1, aMSL2, aMSL3, aMOF, and aMLE antibodies were previously described in Refs [12,[32][33][34]. aSXL antibody was kindly provided by F. Gebauer and previously described in Ref.…”

Section: Rna-seq Data Analysismentioning

confidence: 99%

“…Key to targeting of the X are genetically encoded DCC binding sites, which are termed chromosomal entry sites (CES; [5,6]) or high-affinity sites (HAS; [7,8]). DCC is targeted to the X through its DNA binding subunit, MSL2 [9,10], which cooperates with the ubiquitous CLAMP protein for tight binding to so-called MSL response elements (MREs) [11,12]. According to the current model, DCC "spreads" from HAS to transcriptionally active genes in the nuclear vicinity [1,2].…”

Section: Introductionmentioning

confidence: 99%

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Progressive dosage compensation during Drosophila embryogenesis is reflected by gene arrangement

Prayitno¹,

Schauer²,

Regnard³

et al. 2019

EMBO Reports

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In Drosophila melanogaster males, X‐chromosome monosomy is compensated by chromosome‐wide transcription activation. We found that complete dosage compensation during embryogenesis takes surprisingly long and is incomplete even after 10 h of development. Although the activating dosage compensation complex (DCC) associates with the X‐chromosome and MOF acetylates histone H4 early, many genes are not compensated. Acetylation levels on gene bodies continue to increase for several hours after gastrulation in parallel with progressive compensation. Constitutive genes are compensated earlier than developmental genes. Remarkably, later compensation correlates with longer distances to DCC binding sites. This time–space relationship suggests that DCC action on target genes requires maturation of the active chromosome compartment.

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Section: Chromatin Binding Of Msl2 Precedes Complete Dosage Compensationmentioning

confidence: 99%

Section: Rna-seq Data Analysismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Progressive dosage compensation during Drosophila embryogenesis is reflected by gene arrangement

Prayitno¹,

Schauer²,

Regnard³

et al. 2019

EMBO Reports

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“…We explored the interaction between the two recombinant complexes after expression from baculovirus vectors. Extracts containing JJ-complex (FLAG-JIL-1/untagged JASPer) on the one hand and a partial DCC consisting of MSL1, MSL2 and MSL3 (FLAG-MSL1/untagged MSL2/FLAG-MSL3) on the other hand were mixed in appropriate stoichiometry 45 and specific antibodies were used for immunoprecipitation (Supplementary Fig.8d). The MSL1 antibody retrieved not only the associated MSL2 and 3, but also some JJ-complex.…”

Section: Resultsmentioning

confidence: 99%

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

Albig

Wang

Dann

et al. 2019

Preprint

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31In flies, the chromosomal kinase JIL-1 is responsible for most interphase histone H3S10 32 phosphorylation and has been proposed to protect active chromatin from acquiring 33 heterochromatic marks, like dimethylated histone H3K9 (H3K9me2) and HP1. Here, we show 34 that JIL-1's targeting to chromatin depends on a new PWWP domain-containing protein 35JASPer (JIL-1 Anchoring and Stabilizing Protein). The JASPer-JIL-1 (JJ)-complex is the 36 major form of the kinase in vivo and is targeted to active genes and telomeric transposons 37 via binding of the PWWP domain of JASPer to H3K36me3 nucleosomes. Put in place, the 38 complex modulates the transcriptional output. JIL-1 and JJ-complex depletion in cycling cells 39 lead to small changes in H3K9me2 distribution at active genes and telomeric transposons. 40Finally, we identified many new interactors of the endogenous JJ-complex and propose that 41 JIL-1 not only prevents heterochromatin formation, but also coordinates chromatin-based 42 regulation in the transcribed part of the genome. 43 Key Words: PWWP domain / histone phosphorylation / COMPASS / heterochromatin / BOD1 44 / Dpy-30L1 / Telomeres 45 46 Main text 47In mammals, several nuclear kinases contribute to phosphorylation of histone H3 at serine 48 10 (H3S10ph) in interphase, whereas in Drosophila melanogaster, the essential kinase JIL-1 49 is responsible for most of it 1 . The significance of interphase H3S10ph is often 50 underestimated because most H3S10 phosphorylation in asynchronous cell populations 51 stems from mitotic chromatin, where it is deployed by Aurora kinase B 2,3 . Originally, 52interphase H3S10ph has been associated, in combination with H3K9ac and H3K14ac, with 53 transcriptional activation of immediate early genes upon MAPK activation 4,5 . In Drosophila, 54interphase H3S10ph is enriched at the body of active genes 6 . In mammal, in the extreme 55 case of mouse embryonic stem cells (mESC), ~30% of the genome is enriched for H3S10ph 56 in interphase 7 . 57The current model is that JIL-1 protects euchromatin from heterochromatization 8 . According 58 to the phospho-methyl switch model for mitotic H3S10ph 9 , placing H3S10ph prevents H3K9 59 methylation and subsequent binding of heterochromatin components. JIL-1 phosphorylates 60 various H3 peptides with different methylation states, including H3K9me2/3, with a 61 comparable efficiency 6 , whereas histone methyltransferases of the Su(var)3-9 family are 62 inhibited by H3S10ph 10,11 . Several observations suggest that JIL-1 is important for the 63 balance between eu-and heterochromatin. The Su(var)3-1 alleles of JIL-1 gene, which lead 64 to the expression of JIL-1 truncated in its C-terminal domain (CTD), result in reduced 65 heterochromatin spreading at euchromatin-heterochromatin boundaries 12,13 . Conversely, in 66 the JIL-1 z2/z2 null mutant, heterochromatin components spread into euchromatin. The 67 spreading of H3K9me2 and HP1 is highest on the euchromatic part of the X chromosome in 68 both sexes 14 , the spreading of the 7-zinc-finger pr...

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“…of MSL2 to DNA mediated by DNA shape(Albig et al 2019), specific threedimensional conformation surrounding CES(Ramírez et al 2015) , and 1.688 repetitive elements (Joshi and Meller 2017) . In the future, it will be possible to use the meiotic drive system to define the contribution of each of these factors to MSLc targeting in a developmental context.…”

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confidence: 99%

Targeting of the dosage-compensated male X-chromosome during earlyDrosophiladevelopment

Rieder

Jordan

Larschan

2019

Preprint

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The essential process of dosage compensation, which corrects for the imbalance in Xlinked gene expression between XX females and XY males, represents a key model for how genes are targeted for coordinated regulation. However, the mechanism by which dosage compensation complexes identify the Xchromosome during early development remained unknown because of the difficulty of sexing embryos prior to zygotic transcription. We used meiotic drive to sex Drosophila embryos prior to zygotic transcription and ChIPseq to measure dynamics of dosage compensation factor targeting. The Drosophila MaleSpecific Lethal dosage compensation complex (MSLc) requires the ubiquitous zincfinger protein ChromatinLinked Adaptor for MSL Proteins (CLAMP) to identify the Xchromosome. We observe a multistage process in which MSLc first identifies CLAMP binding sites throughout the genome followed by concentration at the strongest Xlinked MSLc sites. We provide insight into the dynamic mechanism by which a large transcription complex identifies its binding sites during early development.

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Factor cooperation for chromosome discrimination inDrosophila

Cited by 37 publications

References 72 publications

Progressive dosage compensation during Drosophila embryogenesis is reflected by gene arrangement

Progressive dosage compensation during Drosophila embryogenesis is reflected by gene arrangement

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

Targeting of the dosage-compensated male X-chromosome during earlyDrosophiladevelopment

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