IdAnoMacuDA_375_x
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ABSTRACT:
PROVIDER: PRJEB53251 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Anopheles maculipalpis genome assembly, idAnoMacuDA_375_x, alternate haplotype
| PRJEB53252 | ENA
Project description:Anopheles maculipalpis principal pseudohaplotype genome sequencing
| PRJNA830731 | ENA
Project description:Anopheles maculipalpis alternate pseudohaplotype genome sequencing
| PRJNA830730 | ENA
Project description:Anopheles maculipalpis, genomic and transcriptomic data
| PRJEB51755 | ENA
Project description:Malaria morbidity and mortality caused by both Plasmodium falciparum and Plasmodium vivax extend well beyond the African continent, and, although P. vivax causes 80-300 million severe cases each year, vivax transmission remains poorly understood. Plasmodium parasites are transmitted by Anopheles mosquitoes, and the critical site of interaction between parasite and host is at the mosquito's luminal midgut brush border. While the genome of the "model" African P. falciparum vector, Anopheles gambiae, has been sequenced, evolutionary divergence limits its utility as a reference across anophelines, especially non-sequenced P. vivax vectors such as Anopheles albimanus. Clearly, enabling technologies and platforms that bridge this substantial scientific gap are required in order to provide public health scientists key transcriptomic and proteomic information that could spur the development of novel interventions to combat this disease. To our knowledge, no approaches have been published which address this issue. To bolster our understanding of P. vivax-An. albimanus midgut interactions, we developed an integrated bioinformatic-hybrid RNA-Seq-LC-MS/MS approach involving An. albimanus transcriptome (15,764 contigs) and luminal midgut subproteome (9,445 proteins) assembly, which, when used with our custom Diptera protein database (685,078 sequences), facilitated a comparative proteomic analysis of the midgut brush borders of two important malaria vectors, An. gambiae and An. albimanus. Summary from: http://www.mcponline.org/content/early/2012/10/17/mcp.M112.019596.long The An. albimanus transcriptome dataset is available at http://funcgen.vectorbase.org/RNAseq/Anopheles_albimanus/INSP/v2
2012-11-02 | PXD000062 | Pride
Project description:Heteromorphic sex chromosomes induce potentially deleterious gene expression imbalances that are frequently corrected by dosage compensation (DC). Three distinct molecular strategies to achieve DC have been previously described in nematodes, fruit flies and mammals. The reason for these mechanistic differences remain unclear: Are they a consequence of distinct genomes and gene content, functional or ecological constraints, or random initial commitment to an evolutionary trajectory? Here, we study DC in the malaria mosquito Anopheles gambiae. The X chromosomes of Anopheles and Drosophila evolved independently, yet from the same ancestral autosome and share a high degree of homology. We find that Anopheles achieves DC by an entirely different mechanism compared to the MSL complex - H4K16ac axis operating in Drosophila. CRISPR knock-out of msl-2 in Anopheles leads to early embryonic lethality and affects both sexes. Transcriptome analyses indicate that this phenotype is not a consequence of defective X chromosome DC, but instead relates to misregulation of developmental genes. Furthermore, Histone H4 Lysine 16 acetylation does not mark an X chromosome territory, neither does it display a sexually dimorphic genome-wide distribution by ChIP. We conclude that a novel pathway confers X chromosome upregulation in male Anopheles. Our findings highlight the pluralism of how organisms cope with gene-dosage alterations and show that different mechanisms can evolve even in scenarios of highly similar genomic and functional constraints.
2021-05-31 | GSE153778 | GEO
Project description:Malaria-transmitting mosquitoes are extremely sexually dimorphic in their anatomy and behaviour. Sex-specific gene expression in Anopheles gambiae is well-studied in adult stages, but its onset during embryogenesis, apart from sex-determination factors like Yob, remains largely unknown. Here, we report a comprehensive single-embryo transcriptome atlas of A. gambiae males and females to understand the earliest stages of establishing the sex-specific expression networks. Our dataset reveals embryonic RNA isoform diversity including a global shift towards distal alternative polyadenylation (APA) events sites during the maternal-to-zygotic genome transition. Sex-biased gene expression and alternative splicing are limited during embryogenesis, with most sex-specific patterns emerging post-embryonically. X chromosome dosage compensation is established shortly after zygotic genome activation concomitant with direct binding of the master regulator protein SOA to X-linked promoters. In contrast to DC regulators in Drosophila and mammals, we find rather weak evidence in Anopheles for early binding sites or distance-dependent patterns. Instead, both compensation and binding tend to occur locally and uniformly across genes and developmental stages. The most highly expressed genes tend to show the strongest SOA binding. We propose that the Anopheles dosage compensation system represents an extreme case of a gene-by-gene regulatory mechanism that operates at the chromosome-wide level.
2025-05-13 | GSE297043 | GEO
Project description:Malaria-transmitting mosquitoes are extremely sexually dimorphic in their anatomy and behaviour. Sex-specific gene expression in Anopheles gambiae is well-studied in adult stages, but its onset during embryogenesis, apart from sex-determination factors like Yob, remains largely unknown. Here, we report a comprehensive single-embryo transcriptome atlas of A. gambiae males and females to understand the earliest stages of establishing the sex-specific expression networks. Our dataset reveals embryonic RNA isoform diversity including a global shift towards distal alternative polyadenylation (APA) events sites during the maternal-to-zygotic genome transition. Sex-biased gene expression and alternative splicing are limited during embryogenesis, with most sex-specific patterns emerging post-embryonically. X chromosome dosage compensation is established shortly after zygotic genome activation concomitant with direct binding of the master regulator protein SOA to X-linked promoters. In contrast to DC regulators in Drosophila and mammals, we find rather weak evidence in Anopheles for early binding sites or distance-dependent patterns. Instead, both compensation and binding tend to occur locally and uniformly across genes and developmental stages. The most highly expressed genes tend to show the strongest SOA binding. We propose that the Anopheles dosage compensation system represents an extreme case of a gene-by-gene regulatory mechanism that operates at the chromosome-wide level.
2025-05-13 | GSE297010 | GEO