BioProject PRJNA381064: Convergent origination of a Drosophila-like dosage compensation mechanism in a reptile lineage (Allelic Gene Expression in Anolis carolinensis, single-cell RNA-seq)
Ontology highlight
ABSTRACT:
ORGANISM(S): Anolis carolinensis
PROVIDER: GSE100976 | GEO | 2017/10/27
REPOSITORIES: GEO
Similar Datasets
Project description:In order to rule out the presence of imprinted X inactivation in A. carolinensis females we generated RNA-seq data from brain, heart, kidney, liver, ovary and genome sequence data from kidney.
2017-12-04 | GSE107602 | GEO
Project description:In order to study the green anole dosage compensation mechanism we generated strand-specific RNA-seq libraries for a total of 186 samples from the green anole and other representative amniotes (human, mouse, opossum, platypus, chicken and xenopus). Moreover, in order to understand the dosage compensation mechanism of A. carolinensis, we generated ChIP-Seq data for the histone modification H4K16ac and compared levels of acetylation between males and females. Moreover, we reconstructed 7 Y-linked transcripts of Anolis carolinensis based on a male/female subtraction approach and validate these Y sequences using re-sequenced genomes.
2017-10-27 | GSE97367 | GEO
Project description:Sex chromosomes differentiated from different ancestral autosomes in various vertebrate lineages. Here, we trace the functional evolution of the XY Chromosomes of the green anole lizard (Anolis carolinensis), on the basis of extensive high-throughput genome, transcriptome and histone modification sequencing data and revisit dosage compensation evolution in representative mammals and birds with substantial new expression data. Our analyses show that Anolis sex chromosomes represent an ancient XY system that originated at least ≈160 million years ago in the ancestor of Iguania lizards, shortly after the separation from the snake lineage. The age of this system approximately coincides with the ages of the avian and two mammalian sex chromosomes systems. To compensate for the almost complete Y Chromosome degeneration, X-linked genes have become twofold up-regulated, restoring ancestral expression levels. The highly efficient dosage compensation mechanism of Anolis represents the only vertebrate case identified so far to fully support Ohno's original dosage compensation hypothesis. Further analyses reveal that X up-regulation occurs only in males and is mediated by a male-specific chromatin machinery that leads to global hyperacetylation of histone H4 at lysine 16 specifically on the X Chromosome. The green anole dosage compensation mechanism is highly reminiscent of that of the fruit fly, Drosophila melanogaster Altogether, our work unveils the convergent emergence of a Drosophila-like dosage compensation mechanism in an ancient reptilian sex chromosome system and highlights that the evolutionary pressures imposed by sex chromosome dosage reductions in different amniotes were resolved in fundamentally different ways.
| S-EPMC5741051 | biostudies-literature
Project description:Allele-specific gene expression have been observed in genomic imprinting, X chromosome inactivation, allelic exclusion of immunoglobulin loci and non-canonical random monoallelic expression. Here we show that MSL2 can regulate allele specific gene expression and we elucidate its mechanism of action. MSL2 is known to regulate gene dosage up to two fold in drosophila and mammals. In addition to its canonical role as a milder modulator, we found that the loss of MSL2 switches off gene expression completely in an allele specific way and results in biallelic to monoallelic gene expression, which will be ignored as classical down regulated genes without applying the mouse hybrid F1 system. It indicates that MSL2 can activate the expression of the allele which is otherwise inactive intrinsically. We further found this is achieved by the interplay between MSL and KANSL complex. MSL2 acts as a methylation-insensitive factor, which can prevent DNA methylation of the inactive allele, thus facilitating occupancy of methylation-sensitive factor KANSL3 and activating the gene expression. The novel mechanism of MSL2 provides a safeguarding system to warrant biallelic gene expression of intrinsically monoallelic expressed genes including X-inactivated and imprinting genes. These genes are further discovered as sex bias genes such as X-inactivation escaped genes (escapees) are expressed higher in females. Furthermore, the biallelic expression of MSL2 regulated escapees may protect females from single loss of function mutation and contribute to male severer or predominance neurodevelopmental diseases.
2023-08-10 | GSE231588 | GEO
Project description:Allele-specific gene expression have been observed in genomic imprinting, X chromosome inactivation, allelic exclusion of immunoglobulin loci and non-canonical random monoallelic expression. Here we show that MSL2 can regulate allele specific gene expression and we elucidate its mechanism of action. MSL2 is known to regulate gene dosage up to two fold in drosophila and mammals. In addition to its canonical role as a milder modulator, we found that the loss of MSL2 switches off gene expression completely in an allele specific way and results in biallelic to monoallelic gene expression, which will be ignored as classical down regulated genes without applying the mouse hybrid F1 system. It indicates that MSL2 can activate the expression of the allele which is otherwise inactive intrinsically. We further found this is achieved by the interplay between MSL and KANSL complex. MSL2 acts as a methylation-insensitive factor, which can prevent DNA methylation of the inactive allele, thus facilitating occupancy of methylation-sensitive factor KANSL3 and activating the gene expression. The novel mechanism of MSL2 provides a safeguarding system to warrant biallelic gene expression of intrinsically monoallelic expressed genes including X-inactivated and imprinting genes. These genes are further discovered as sex bias genes such as X-inactivation escaped genes (escapees) are expressed higher in females. Furthermore, the biallelic expression of MSL2 regulated escapees may protect females from single loss of function mutation and contribute to male severer or predominance neurodevelopmental diseases.
2023-08-10 | GSE227741 | GEO
Project description:The repeatability or predictability of evolution is a central question in evolutionary biology and most often addressed in experimental evolution studies. Here, we infer how genetically heterogeneous natural systems acquire the same molecular changes to address how genomic background affects adaptation in natural populations. In particular, we take advantage of independently formed neo-sex chromosomes in Drosophila species that have evolved dosage compensation by co-opting the dosage-compensation male-specific lethal (MSL) complex to study the mutational paths that have led to the acquisition of hundreds of novel binding sites for the MSL complex in different species. This complex recognizes a conserved 21-bp GA-rich sequence motif that is enriched on the X chromosome, and newly formed X chromosomes recruit the MSL complex by de novo acquisition of this binding motif. We identify recently formed sex chromosomes in the D. melanica and D. robusta species groups by genome sequencing and generate genomic occupancy maps of the MSL complex to infer the location of novel binding sites. We find that diverse mutational paths were utilized in each species to evolve hundreds of de novo binding motifs along the neo-X, including expansions of microsatellites and transposable element (TE) insertions. However, the propensity to utilize a particular mutational path differs between independently formed X chromosomes and appears to be contingent on genomic properties of that species, such as simple repeat or TE density. This establishes the "genomic environment" as an important determinant in predicting the outcome of evolutionary adaptations.
| S-EPMC6417741 | biostudies-literature
Project description:Coping with variations in network dosage is crucial for maintaining optimal function in gene networks. We explored how network structure facilitates network-level dosage compensation. By using the yeast galactose network as a model, we combinatorially deleted one of the two copies of its four regulatory genes and found that network activity was robust to the change in network dosage. A mathematical analysis revealed that a two-component genetic circuit with elements of opposite regulatory activity (activator and inhibitor) constitutes a minimal requirement for network-dosage invariance. Specific interaction topologies and a one-to-one interaction stoichiometry between the activating and inhibiting agents were additional essential elements facilitating dosage invariance. This mechanism of network-dosage invariance could represent a general design for gene network structure in cells.
| S-EPMC3138731 | biostudies-literature
Project description:The Anopheles mosquito is one of thousands of species in which sex differences play a central role in their biology, as only females need a blood meal in order to produce eggs. Sex differentiation is regulated by sex chromosomes, but their presence creates a dosage imbalance between males (XY) and females (XX). Dosage compensation (DC) can re-equilibrate the expression of sex-chromosomal genes, but because the molecular mechanisms providing DC have only been studied in a few model organisms, key questions about its evolutionary diversity and functional necessity remain unresolved. Here, we reveal the DC pathway in the malaria mosquito Anopheles gambiae. We identified SOA, a previously uncharacterized gene, whose expression is sufficient to induce a global upregulation of X-linked genes. Sex-specific alternative splicing prevents the production of a functional SOA protein in females. The male SOA isoform encodes a DNA-binding protein that recognizes the promoters of X chromosomal genes through a CA repeat sequence. Male mosquitos lacking SOA exhibit a chromosome-wide downregulation of the X, which is compatible with viability, but causes a developmental delay. Thus, our molecular analysis of the first DC master regulator in a non-model organism elucidates the evolutionary steps leading to the establishment of a chromosome-specific fine-tuning mechanism.
2023-07-13 | PXD042353 | Pride
Project description:We have conducted a global analysis of somatic dosage compensation and also asked if germ cell dosage compensate by microarray analysis of gene expression in wild-type tissues. To obviate the confounding effects of scatter and especially the skewed genomic distributions of genes with sex-biased expression in both the soma and germline [there are fewer X chromosome genes with male-biased expression], we used mutations that transform sexual identity. In the soma we used gain-of-function transformer to turn X;AA flies into somatic females with tumorous germlines. The gonadectomized somas of these X;AA female flies were compared to similarly prepared XX;AA females. The X;AA ovarian tumors, which are possibly the result of germline sex transformations, were compared to the similar XX;AA ovarian tumors generated with loss-of-function alleles of ovarian tumor and Sex-lethal. We used alleles of transformer-2 and doublesex to transform XX;AA flies into somatic males with atrophic germlines. Keywords: other
2005-12-15 | GSE2119 | GEO
Project description:Gene dosage imbalance of heteromorphic sex chromosomes (XY or ZW) exists between the sexes, and with the autosomes. Mammalian X chromosome inactivation was long thought to imply a critical need for dosage compensation in vertebrates. However, mRNA abundance measurements that demonstrated sex chromosome transcripts are neither balanced between the sexes or with autosomes in monotreme mammals or birds brought sex chromosome dosage compensation into question. This study examines transcriptomic and proteomic levels of dosage compensation in platypus and chicken compared to mouse, a model eutherian species. We analyzed mRNA and protein levels in heart and liver tissues of chicken, mouse and platypus.
2024-07-30 | PXD040182 | Pride