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Hartke, J.

Publications and source records attributed to Hartke, J..

3 recordsLinked to original sources

The influence of parasite load on transcriptional activity and morphology of a cestode and its ant intermediate host

Parasites with complex life cycles are known to induce phenotypic changes in their intermediate hosts to increase transmission to the final host. The magnitude of these changes could increase with the number of parasites, which would be beneficial to co-infecting parasites. Yet, adverse effects of high parasite load (i.e., many parasites in a single host) might stress both hosts and parasites (e.g., through an increased immune response). We investigated the consequences of parasite load on the transcriptional activity and morphology of the cestode Anomotaenia brevis and its intermediate host, the ant Temnothorax nylanderi. We demonstrated that many differentially expressed host genes shifted with parasite load, and their functions indicate a stronger immune response and fight against oxidative stress in heavily infected hosts. The expression of other host genes responded to infection in an all-or-nothing manner, as did the morphology of the host workers. However, the cestodes became smaller when they competed with other parasites for resources from a single host. Their expression profile further indicated shifts in host immune avoidance, starvation resistance and vesicle-mediated transport. In summary, our study reveals clear consequences of parasite load and highlights specific processes and traits affected by this.

evolutionary biology↗

What doesn't kill you makes you live longer - Longevity of a social host linked to parasite proteins

Parasites with complex lifecycles often manipulate the phenotype of their intermediate hosts to increase the probability of transmission to their definitive hosts. Infection with Anomotaenia brevis, a cestode that uses Temnothorax nylanderi ants as intermediate hosts, leads to a multiple-fold extension of host lifespan and to changes in behaviour, morphology, and colouration. The mechanisms behind these changes are unknown, as is whether the increased longevity is achieved through parasite manipulation. Here we demonstrate that the parasite releases proteins into its host with functions that might explain the observed changes. These parasitic proteins make up a substantial portion of the proteome of the hosts haemolymph, and thioredoxin peroxidase and superoxide dismutase, two antioxidants, exhibited the highest abundances among them. The largest part of the secreted proteins could not be annotated, indicating they are either novel or severely altered during recent coevolution to function in host manipulation. We also detected shifts in the hosts proteome with infection, in particular an overabundance of vitellogenin-like-A in infected ants, a protein that regulates division of labour in Temnothorax ants, which could explain the observed behavioural changes. Our results thus point at two different strategies likely employed by this parasite to manipulate its host - by secretion of proteins with immediate influence on the hosts phenotype and by altering the hosts translational activity. Our findings reveal the intricate molecular interplay required to influence the phenotype of a host and shed light on potential signalling pathways and genes involved in parasite-host communication.

evolutionary biology↗

Genomic profiling of climate adaptation in Aedes aegypti along an altitudinal gradient in Nepal indicates non-gradual expansion of the disease vector

BackgroundDriven by globalization, urbanization and climate change, the distribution range of invasive vector species has expanded to previously colder ecoregions. To reduce health-threatening impacts on humans, insect vectors are extensively studied. Population genomics can reveal the genomic basis of adaptation and help to identify emerging trends of vector expansion. ResultsBy applying whole genome analyses and genotype-environment associations to populations of the main dengue vector Ae. aegypti, sampled along an altitudinal temperature gradient in Nepal (200- 1300m), we identify adaptive traits and describe the species genomic footprint of climate adaptation to colder ecoregions. We found two clusters of differentiation with significantly different allele frequencies in genes associated to climate adaptation between the highland population (1300m) and all other lowland populations ([≤] 800 m). We revealed non-synonymous mutations in 13 of the candidate genes associated to either altitude, precipitation or cold tolerance and identified an isolation-by-environment differentiation pattern. ConclusionOther than the expected gradual differentiation along the altitudinal gradient, our results reveal a distinct genomic differentiation of the highland population. This finding either indicates a differential invasion history to Nepal or local high-altitude adaptation explaining the populations phenotypic cold tolerance. In any case, this highland population can be assumed to carry pre-adapted alleles relevant for the species invasion into colder ecoregions worldwide that way expanding their climate niche.

genomics↗