Transcriptional modulation of entire chromosomes: dosage compensation

Lucchesi, John C.

doi:10.1007/s12041-018-0919-7

Cited by 25 publications

(23 citation statements)

References 98 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous studies on dosage compensation in model organisms indicate that chromatin structure plays a key role in the regulation of this evolutionary mechanism (Lucchesi et al. 2005; Lucchesi 2018). As the main transcriptomic differences were observed between the free stage cercariae and the intravertebrate stages, we focused our epigenetic study on cercariae and immature worms.…”

Section: Resultsmentioning

confidence: 99%

“…In particular, well-studied chromosome-wide mechanisms of dosage compensation are characterized by global and extensive changes in the epigenetic landscape of the affected sex chromosome (Lucchesi et al. 2005; Lucchesi 2018). For instance, active chromatin marks are strongly enriched on the Drosophila male X, whereas the inactivated mammalian X chromosome of females is characterized by DNA methylation and widespread repressive chromatin marks (Lucchesi et al.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Dosage Compensation throughout the Schistosoma mansoni Lifecycle: Specific Chromatin Landscape of the Z Chromosome

Picard

Vicoso

Roquis

et al. 2019

Genome Biology and Evolution

View full text Add to dashboard Cite

Differentiated sex chromosomes are accompanied by a difference in gene dose between X/Z-specific and autosomal genes. At the transcriptomic level, these sex-linked genes can lead to expression imbalance, or gene dosage can be compensated by epigenetic mechanisms and results into expression level equalization. Schistosoma mansoni has been previously described as a ZW species (i.e., female heterogamety, in opposition to XY male heterogametic species) with a partial dosage compensation, but underlying mechanisms are still unexplored. Here, we combine transcriptomic (RNA-Seq) and epigenetic data (ChIP-Seq against H3K4me3, H3K27me3, and H4K20me1 histone marks) in free larval cercariae and intravertebrate parasitic stages. For the first time, we describe differences in dosage compensation status in ZW females, depending on the parasitic status: free cercariae display global dosage compensation, whereas intravertebrate stages show a partial dosage compensation. We also highlight regional differences of gene expression along the Z chromosome in cercariae, but not in the intravertebrate stages. Finally, we feature a consistent permissive chromatin landscape of the Z chromosome in both sexes and stages. We argue that dosage compensation in schistosomes is characterized by chromatin remodeling mechanisms in the Z-specific region.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Dosage Compensation throughout the Schistosoma mansoni Lifecycle: Specific Chromatin Landscape of the Z Chromosome

Picard

Vicoso

Roquis

et al. 2019

Genome Biology and Evolution

View full text Add to dashboard Cite

show abstract

“…In Drosophila males, a multisubunit dosage compensation complex (DCC) is responsible for a precise compensatory increase in the expression of genes on the X chromosome (Kuroda et al, 2016;Lucchesi, 2018;Samata and Akhtar, 2018). The DCC consists of five proteins, MSL1, MSL2, MSL3, MOF and MLE, and includes two redundant non-coding RNAs, roX1 (3.7 kb) and roX2 (0.6 kb) that perform similar functions (Lucchesi, 2018;Samata and Akhtar, 2018). MSL2 is expressed only in males and is the core DCC component, suggesting a key role in binding specificity of DCC to the X chromosome (Kuroda et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

The simultaneous interaction of MSL2 with CLAMP and DNA provides redundancy in the initiation of dosage compensation in Drosophila males

et al. 2019

View full text Add to dashboard Cite

The binding of the Drosophila male-specific lethal dosage compensation complex (DCC) exclusively to the male X chromosome provides an excellent model system to understand mechanisms of selective recruitment of protein complexes to chromatin. Previous studies showed that the male-specific organizer of the complex, MSL2, and the ubiquitous DNA-binding protein CLAMP are key players in the specificity of X chromosome binding. The CXC domain of MSL2 binds to genomic sites of DCC recruitment in vitro. Another conserved domain of MSL2, named Clamp-binding domain (CBD) directly interacts with the N-terminal zinc-finger domain of CLAMP. Here, we found that inactivation of CBD or CXC individually only modestly affected recruitment of the DCC to the X chromosome in males. However, combination of these two genetic lesions within the same MSL2 mutant resulted in an increased loss of DCC recruitment to the X chromosome. Thus, proper MSL2 positioning requires an interaction with either CLAMP or DNA to initiate dosage compensation in Drosophila males.

show abstract

“…Thus, monosomy of the relatively gene-rich X chromosome in the heterogametic sex (XY) poses a dosage problem that needs to be resolved. Diverse mechanisms have evolved to address the sex chromosome gene dosage imbalance (Mank, 2013; Disteche, 2016; Graves, 2016; Gu and Walters, 2017; Lucchesi, 2018; Samata and Akhtar, 2018). In Drosophila melanogaster , to compensate for the X monosomy in males, a mechanism known as complete dosage compensation works by hyper-expressing the entire X chromosome to equalize gene expression with that of females having two X chromosomes.…”

Section: Introductionmentioning

confidence: 99%

Guy1, a Y-linked embryonic signal, regulates dosage compensation in Anopheles stephensi by increasing X gene expression

Saunders

et al. 2019

eLife

View full text Add to dashboard Cite

We previously showed that Guy1, a primary signal expressed from the Y chromosome, is a strong candidate for a male-determining factor that confers female-specific lethality in Anopheles stephensi (Criscione et al., 2016). Here, we present evidence that Guy1 increases X gene expression in Guy1-transgenic females from two independent lines, providing a mechanism underlying the Guy1-conferred female lethality. The median level gene expression (MGE) of X-linked genes is significantly higher than autosomal genes in Guy1-transgenic females while there is no significant difference in MGE between X and autosomal genes in wild-type females. Furthermore, Guy1 significantly upregulates at least 40% of the 996 genes across the X chromosome in transgenic females. Guy1-conferred female-specific lethality is remarkably stable and completely penetrant. These findings indicate that Guy1 regulates dosage compensation in An. stephensi and components of dosage compensation may be explored to develop novel strategies to control mosquito-borne diseases.

show abstract

Transcriptional modulation of entire chromosomes: dosage compensation

Cited by 25 publications

References 98 publications

Dosage Compensation throughout the Schistosoma mansoni Lifecycle: Specific Chromatin Landscape of the Z Chromosome

Dosage Compensation throughout the Schistosoma mansoni Lifecycle: Specific Chromatin Landscape of the Z Chromosome

The simultaneous interaction of MSL2 with CLAMP and DNA provides redundancy in the initiation of dosage compensation in Drosophila males

Guy1, a Y-linked embryonic signal, regulates dosage compensation in Anopheles stephensi by increasing X gene expression

Contact Info

Product

Resources

About