Laupala
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA892786 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Parallel Evolution of Four Laupala Species
| PRJNA891623 | ENA
Project description:Differential gene expression and misregulation in Laupala kohalensis x Laupala paranigra F2 hybrids
| PRJNA892886 | ENA
Project description:Laupala cerasina Transcriptome or Gene expression
| PRJNA429662 | ENA
Project description:Laupala kohalensis isolate:Lakoh051 Genome sequencing and assembly
| PRJNA392944 | ENA
Project description:Rapid parallel adaptation despite gene flow in silent crickets
| PRJEB39125 | ENA
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.
2020-06-02 | GSE151539 | GEO
Project description:Genomics of Rapid Evolution in Field Crickets
| PRJEB24786 | ENA
Project description:The loss of the tail is one of the main anatomical evolutionary changes to have occurred along the lineage leading to humans and to the “anthropomorphous apes”. This morphological evolution in the ancestral hominoids has long been considered to have accommodated a characteristic style of locomotion and contributed to the evolution of bipedalism in humans. Yet, the genetic mechanism that facilitated tail-loss evolution in hominoids remains unknown. Primate genome sequencing projects have made possible the inference of causal links between genotypic and phenotypic changes, and enabled the search for hominoid-specific genetic elements controlling tail development. Here, we present evidence that an individual Alu element insertion in the genome of the hominoid ancestor may have contributed to tail-loss evolution. We demonstrate that this Alu element – inserted into an intron of the TBXT gene (also called T or Brachyury ) – pairs with a neighboring ancestral Alu element encoded in the reverse genomic orientation and leads to a hominoid-specific alternative splicing event. To study the effect of this splicing event, we generated multiple mouse models that express both full length and exon-skipped isoforms of mouse Tbxt, mimicking expression pattern of its hominoid ortholog TBXT. We found that mice expressing both Tbxt isoforms can exhibit a complete absence of the tail or a shortened tail, depending on the relative abundance of Tbxt isoforms expressed at the embryonic tail bud, supporting the notion that the exon-skipped transcript is sufficient to induce a tail-loss phenotype. We further noted that mice expressing the exon-skipped Tbxt isoform – both in heterozygous and homozygous forms – may develop a neural tube defect condition, which affects ~1/1,000 human neonates. We speculate that tail loss evolution along the hominoid lineage may be associated with an adaptive cost of potential neural tube defects that may continue to affect human health today.
2024-01-01 | GSE252196 | GEO