IdAnoMacuDA_375_x
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB53251 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| CALSDU01.dat.gz | Other | |||
| CALSDU01.fasta.gz | Fasta.gz | |||
| CALSDU01.master.dat | Other |
Items per page: 5 1 - 4 of 4 |
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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.
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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
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Project description:Anopheles arabiensis and Anopheles coluzzii genome sequencing and assembly
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