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Progressive dosage compensation during Drosophila embryogenesis is reflected by gene arrangement.

ABSTRACT: 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.

SUBMITTER: Prayitno K

PROVIDER: S-EPMC6680166 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature

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Progressive dosage compensation during Drosophila embryogenesis is reflected by gene arrangement.

Prayitno Khairunnadiya K Schauer Tamás T Regnard Catherine C Becker Peter B PB

EMBO reports 20190709 8

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 gastrul ...[more]

PMID: 31286660

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Progressive dosage compensation during Drosophila embryogenesis is reflected by gene arrangement on the X chromosome

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-06-28 | GSE127177 | GEO

Progressive dosage compensation during Drosophila embryogenesis is reflected by gene arrangement on the X chromosome [RNA-seq]

Project description:In D. melanogaster males, X chromosome monosomy is compensated by chromosome-wide transcription activation. We found that complete dosage compensation during embryogenesis takes surprisingly long. Although the activating Dosage Compensation Complex (DCC) associates with the chromosome and 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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Progressive dosage compensation during Drosophila embryogenesis is reflected by gene arrangement on the X chromosome [ChIP-seq]

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Progressive dosage compensation during Drosophila embryogenesis is reflected by gene arrangement on the X chromosome

Project description:Progressive dosage compensation during Drosophila embryogenesis is reflected by gene arrangement on the X chromosome

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Progressive dosage compensation during Drosophila embryogenesis is reflected by gene arrangement on the X chromosome [ChIP-seq]

Project description:Progressive dosage compensation during Drosophila embryogenesis is reflected by gene arrangement on the X chromosome [ChIP-seq]

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Progressive dosage compensation during Drosophila embryogenesis is reflected by gene arrangement on the X chromosome [RNA-seq]

Project description:Progressive dosage compensation during Drosophila embryogenesis is reflected by gene arrangement on the X chromosome [RNA-seq]

| PRJNA524294 | ENA

Male-Killing Spiroplasma Alters Behavior of the Dosage Compensation Complex during Drosophila melanogaster Embryogenesis.

Project description:Numerous arthropods harbor maternally transmitted bacteria that induce the preferential death of males [1-7]. This sex-specific lethality benefits the bacteria because males are "dead ends" regarding bacterial transmission, and their absence may result in additional resources for their viable female siblings who can thereby more successfully transmit the bacteria [5]. Although these symbionts disrupt a range of developmental processes [8-10], the underlying cellular mechanisms are largely unknown. It was previously shown that mutations in genes of the dosage compensation pathway of Drosophila melanogaster suppressed male killing caused by the bacterium, Spiroplasma [10]. This result suggested that dosage compensation is a target of Spiroplasma. However, it remains unclear how this pathway is affected, and whether the underlying interactions require the male-specific cellular environment. Here, we investigated the cellular basis of male embryonic lethality in D. melanogaster induced by Spiroplasma. We found that the dosage compensation complex (DCC), which acetylates X chromatin in males [11], becomes mis-localized to ectopic regions of the nucleus immediately prior to the killing phase. This effect was accompanied by inappropriate histone acetylation and genome-wide mis-regulation of gene expression. Artificially induced formation of the DCC in infected females, through transgenic expression of the DCC-specific gene msl-2, resulted in mis-localization of this complex to non-X regions and early Spiroplasma-induced death, mirroring the killing effects in males. These findings strongly suggest that Spiroplasma initiates male killing by targeting the dosage compensation machinery directly and independently of other cellular features characteristic of the male sex.

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Chromosome-wide gene-specific targeting of the Drosophila dosage compensation complex.

Project description:The dosage compensation complex (DCC) of Drosophila melanogaster is capable of distinguishing the single male X from the other chromosomes in the nucleus. It selectively interacts in a discontinuous pattern with much of the X chromosome. How the DCC identifies and binds the X, including binding to the many genes that require dosage compensation, is currently unknown. To identify bound genes and attempt to isolate the targeting cues, we visualized male-specific lethal 1 (MSL1) protein binding along the X chromosome by combining chromatin immunoprecipitation with high-resolution microarrays. More than 700 binding regions for the DCC were observed, encompassing more than half the genes found on the X chromosome. In addition, several rare autosomal binding sites were identified. Essential genes are preferred targets, and genes binding high levels of DCC appear to experience the most compensation (i.e., greatest increase in expression). DCC binding clearly favors genes over intergenic regions, and binds most strongly to the 3' end of transcription units. Within the targeted genes, the DCC exhibits a strong preference for exons and coding sequences. Our results demonstrate gene-specific binding of the DCC, and identify several sequence elements that may partly direct its targeting.

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Targeting determinants of dosage compensation in Drosophila.

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The Drosophila over compensating males gene genetically inhibits dosage compensation in males.

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| S-EPMC3615101 | biostudies-literature

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