Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR472740_1.fastq.gz | Fastqsanger.gz | |||
| ERR472740_2.fastq.gz | Fastqsanger.gz | |||
| ERR472741_1.fastq.gz | Fastqsanger.gz | |||
| ERR472741_2.fastq.gz | Fastqsanger.gz | |||
| ERR472742_1.fastq.gz | Fastqsanger.gz |
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Project description:Genomics of Rapid Evolution in Field Crickets
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Project description:Organisms possess highly adaptive defence systems to silence rapidly evolving mobile genetic elements such as transposons. While individual transposons may appear and disappear over time, the evolutionary stability of the defence pathways targeting them remains unclear. In the ovarian somatic cells of Drosophila, envelope-carrying gypsy LTR retrotransposons are silenced by the piRNA pathway, which relies solely on Piwi - an evolutionary derivative of an Aubergine/Piwi gene duplication specific to flies. Recent studies, however, have revealed that envelope-carrying gypsy elements are widespread across metazoans and particularly abundant in insect genomes. This prompted us to investigate whether and how the piRNA pathway targets ovarian somatic gypsy elements in other insects. We found that Aedes and Anopheles mosquitoes, as well as stingless bees and crickets, all express piRNAs targeting gypsy elements in ovarian somatic cells, indicating a continuous arms race for more than 400 million years of insect evolution. Interestingly, we found that Aedes aegypti activate the same set of piRNA clusters in ovarian somatic cells as in other somatic tissues where they are known to target RNA viruses. This suggests that piRNA-based antiviral defence in mosquitoes may have originated from the ovarian somatic piRNA pathway. Moreover, we discovered that the mechanisms of piRNA biogenesis in ovarian somatic cells differ among insects: slicing-independent phasing dominates in dipterans, ping-pong amplification in bees, and slicing-dependent phasing in crickets. These findings indicate that distinct piRNA pathways have independently evolved at different timepoints to silence the same class of retrotransposons in insect evolution.
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Project description:Rapid parallel adaptation despite gene flow in silent crickets
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Project description:Among the parasites of insects, endoparasitoids impose a costly challenge to host defenses because they use their host’s body for the development and maturation of their eggs or larvae, and ultimately kill the host. Tachinid flies are highly specialized acoustically-orienting parasitoids that release first instar mobile larvae which burrow into the host’s body to feed. We investigated the possibility that Teleogryllus oceanicus field crickets employ post-infestation strategies to maximize survival when infested with the larvae of the parasitoid fly Ormia ochracea. Using crickets from the Hawaiian island of Kauai, where the parasitoid is present, and crickets from the Cook Islands (Mangaia), where the parasitoid is absent, we evaluated fitness consequences of infestation by comparing feeding behavior, reproductive capacity, and survival of males experimentally infested with O. ochracea larvae. We also evaluated genetic mechanisms underlying host responses by comparing gene expression in crickets infested with fly larvae for different lengths of time with that of uninfested control crickets. We observe some differences in fitness (spermatophore production) and survival (total survival time post-infestation) between populations. However, for both traits significant population effects 1) were not associated with the slope of the response to different numbers of larvae and 2) only emerged from models containing body condition at one but not both time points evaluated. Gene expression patterns also revealed population differences in response to infestation. We did not find evidence for consistent differences in genes associated with immunity or stress response. Taken together, these results suggest that coevolution with the fly does not strongly select for either post-infestation resistance or tolerance of parasitoid larvae in male crickets.
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Project description:The rapid pace of bacterial evolution enables organisms to adapt to the laboratory environment with repeated passage and thus diverge from naturally-occurring environmental (“wild”) strains. Distinguishing wild and laboratory strains is clearly important for biodefense and bioforensics; however, DNA sequence data alone has thus far not provided a clear signature, perhaps due to lack of understanding of how diverse genome changes lead to convergent phenotypes, difficulty in detecting certain types of mutations, or perhaps because some adaptive modifications are epigenetic. Monitoring protein abundance, a molecular measure of phenotype, can overcome some of these difficulties. We have assembled a collection of Yersinia pestis proteomics datasets from our own published and unpublished work, and from a proteomics data archive, and demonstrated that protein abundance data can clearly distinguish laboratory-adapted from wild. We developed a lasso logistic regression classifier that uses binary (presence/absence) or quantitative protein abundance measures to predict whether a sample is laboratory-adapted or wild that proved to be ~98% accurate, as judged by replicated 10-fold cross-validation. Protein features selected by the classifier accord well with our previous study of laboratory adaptation in Y. pestis. The input data was derived from a variety of unrelated experiments and contained significant confounding variables. We show that the classifier is robust with respect to these variables. The methodology is able to discover signatures for laboratory facility and culture medium that are largely independent of the signature of laboratory adaptation. Going beyond our previous laboratory evolution study, this work suggests that proteomic differences between laboratory-adapted and wild Y. pestis are general, potentially pointing to a process that could apply to other species as well. Additionally, we show that proteomics datasets (even archived data collected for different purposes) contain the information necessary to distinguish wild and laboratory samples. This work has clear applications in biomarker detection as well as biodefense.
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Project description:Relapse of acute myeloid leukemia (AML) is highly aggressive and often treatment refractory. We analyzed previously published AML relapse cohorts and found that 40% of relapses occur without changes in driver mutations, suggesting that non-genetic mechanisms drive relapse in a large proportion of cases. We therefore characterized epigenetic patterns of AML relapse using 26 matched diagnosis-relapse samples with ATAC-seq. This analysis identified a relapse-specific chromatin accessibility signature for mutationally stable AML, suggesting that AML undergoes epigenetic evolution at relapse independent of mutational changes. Analysis of leukemia stem cell (LSC) chromatin changes at relapse indicated that this leukemic compartment underwent significantly less epigenetic evolution than non-LSCs, while epigenetic changes in non-LSCs reflected overall evolution of the bulk leukemia. Finally, we used single-cell ATAC-seq paired with mitochondrial sequencing (mtscATAC) to map clones from diagnosis into relapse along with their epigenetic features. We found that distinct mitochondrially-defined clones exhibit more similar chromatin accessibility at relapse relative to diagnosis, demonstrating convergent epigenetic evolution in relapsed AML. These results demonstrate that epigenetic evolution is a feature of relapsed AML and that convergent epigenetic evolution can occur following treatment with induction chemotherapy.
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