Project description:High temperature events can disrupt species interactions, including those among hosts, symbionts, and natural enemies. Understanding the genetic and physiological processes underlying these disruptions is a critical scientific challenge in this era of anthropogenic climate change. We explore how high temperatures disrupt the interactions among an herbivorous insect host, Manduca sexta, its insect parasitoid, Cotesia congregata, and the parasitoid’s symbiotic virus. In this system, high temperatures kill developing parasitoids, but not hosts. We evaluated the physiological and transcriptomic causes of thermal mismatch in ecological interactions using parasitoid egg in vitro experiments, immunological assays, and RNAseq. We found that high temperatures disrupt the capacity of the parasitoid’s symbiotic virus to immunosuppress the host insect, resulting in thermal mismatch and death of the parasitoid. At the transcriptomic level, key viral genes involved in suppressing host immune pathways showed reduced expression, driven by the virus’s circular genomic structure. This work is among the first to demonstrate the genetic and physiological mechanisms by which a symbiont limits the ecological functioning of host-parasite dynamics, and provides a framework for understanding how molecular processes give rise to ecological outcomes in response to high temperature events caused by climate change.
Project description:We explored the transcriptional response to parasitoid attack in Drosophila larvae at nine time points following parasitism, hybridizing five biologic replicates per time point to whole-genome microarrays for both parasitized and control larvae. We found significantly different expression profiles for 159 probe sets (representing genes), and we classified them into 16 clusters based on patterns of co-expression. A series of functional annotations were nonrandomly associated with different clusters, including several involving immunity and related functions. We also identified nonrandom associations of transcription factor binding sites for three main regulators of innate immune responses (GATA/srp-like, NF-kappaB/Rel-like and Stat), as well as a novel putative binding site for an unknown transcription factor. The appearance or absence of candidate genes previously associated with insect immunity in our differentially expressed gene set was surveyed
Project description:The parasitoid wasp Nasonia vitripennis is a major insect model for morphology, behavior, and genetics. It has haplodiploid sex determination: unfertilized eggs develop into haploid males and fertilized eggs develop into diploid females. Additionally, polyploids (diploid males, triploid females) occur in Nasonia, representing gene expression mechanisms regulating sexual maintenance outside of standard haplodiploidy. Here, we generated a transcriptomic atlas for N. vitripennis across two tissues (head and abdomen) for typical haploid males and diploid females and polyploid diploid males and triploid females. These data are a resource for analyses on transcriptomic differences across sex, tissue type, ploidy, strain, and temporal change.
Project description:The parasitoid wasp Nasonia vitripennis is a major insect model for morphology, behavior, and genetics. It has haplodiploid sex determination: unfertilized eggs develop into haploid males and fertilized eggs develop into diploid females. Additionally, polyploids (diploid males, triploid females) occur in Nasonia, representing gene expression mechanisms regulating sexual maintenance outside of standard haplodiploidy. Here, we generated a transcriptomic atlas for N. vitripennis across two tissues (head and abdomen) for typical haploid males and diploid females and polyploid diploid males and triploid females. These data are a resource for analyses on transcriptomic differences across sex, tissue type, ploidy, strain, and temporal change.
Project description:The parasitoid wasp Nasonia vitripennis is a major insect model for morphology, behavior, and genetics. It has haplodiploid sex determination: unfertilized eggs develop into haploid males and fertilized eggs develop into diploid females. Additionally, polyploids (diploid males, triploid females) occur in Nasonia, representing gene expression mechanisms regulating sexual maintenance outside of standard haplodiploidy. Here, we generated a transcriptomic atlas for N. vitripennis across two tissues (head and abdomen) for typical haploid males and diploid females and polyploid diploid males and triploid females. These data are a resource for analyses on transcriptomic differences across sex, tissue type, ploidy, strain, and temporal change.
Project description:The parasitoid wasp Nasonia vitripennis is a major insect model for morphology, behavior, and genetics. It has haplodiploid sex determination: unfertilized eggs develop into haploid males and fertilized eggs develop into diploid females. Additionally, polyploids (diploid males, triploid females) occur in Nasonia, representing gene expression mechanisms regulating sexual maintenance outside of standard haplodiploidy. Here, we generated a transcriptomic atlas for N. vitripennis across two tissues (head and abdomen) for typical haploid males and diploid females and polyploid diploid males and triploid females. These data are a resource for analyses on transcriptomic differences across sex, tissue type, ploidy, strain, and temporal change.
Project description:Parasitoid wasps inject venom to regulate the immune response and development of host arthropods and sometime paralyze host arthropods. Hereby, proteomic method was used to identify putative venom proteins from Theocolax elegans, ectoparasitoids of storage insect pests.
Project description:In insects, sexual differentiation is orchestrated by one transcription factor, Doublesex (DSX). DSX affects Drosophila melanogaster male and female transcriptome, yet how DSX regulates gene expression in other species is unknown. We investigated sex-biased gene expression during juvenile development in the parasitoid wasp Nasonia vitripennis, finding that more than three-quarters of its genes are sex-biased at a certain point in development. Moreover, we transiently knocked down dsx expression to infer its role in sex-specific transcriptome regulation, revealing thousands of affected genes in males and a more subtle effect in females. Finally, we performed an in vitro DNA-protein interaction assay to identify DSX binding sites and primary DSX target genes. By integrating these three datasets, we defined DSX's regulatory function for all genes in N. vitripennis, revealing that DSX acts mainly in males as both an activator and a repressor. This male-centric model for DSX-mediated regulation is likely to apply to many other insect species.
Project description:Cotesia vestalis bracoviruses (CvBVs) are domesticated endogenous viruses (DEVs) derived from ancestral nudiviruses and are integrated into the genome of the parasitoid wasp C. vestalis. The CvBV proviral genome is composed of two distinct components: one encoding genes associated with virion morphogenesis and assembly, and the other harboring virulence genes that are excised, circularized, and packaged into virions. CvBV replication and particle assembly occur exclusively in the ovaries of female wasps. While prior studies have largely focused on the function of virulence genes during parasitization, the molecular mechanisms underlying CvBV replication and assembly have remained largely unknown. In this study, we employed an integrative approach to dissect the CvBV gene set responsible for these processes. We systematically identified 71 conserved nudivirus-like genes in the C. vestalis genome and functionally characterized 21 of them. Among these, three genes involved in transcriptional regulation (p47, lef-5, lef-9) were highlighted. Notably, we discovered three previously unrecognized promoter motifs upstream of CvBV structural genes, revealing novel lineage-specific regulatory elements that may coordinate temporal gene expression via the viral RNA polymerase complex. Additionally, we characterized three CvBV replication-related genes (helicase, integrase-1/-2), eight capsid-related genes (vp39, PmV, HzNVorf9-1, HzNVorf9-2, HzNVorf106, 38k, 27b, K425_459), five genes associated with envelope formation (11k, 17a-1, 35a-1, 35a-2, K425_461), three genes required for virion assembly (vlf-1, HzNVorf140-1, HzNVorf140-2), and two viral infectivity factors (vp91, pif-0). Together, these findings provide the first comprehensive view of the key regulators controlling CvBV production, assembly, and infectivity, offering novel insights into the molecular mechanisms underlying bracovirus biogenesis and the evolutionary divergence of CvBVs from their nudiviral ancestors.