Biology subjects

Hartke, J.

Publications and source records attributed to Hartke, J..

5 recordsLinked to original sources

bioRxiv2026

Multi-omics analysis identifies loci associated with pyrethroid resistance across sister species in the Anopheles gambiae species complex

The Anopheles gambiae species complex includes An. gambiae, An. coluzzii, and An. arabiensis, three of the four major malaria vector species across Africa. Insecticide-based vector control remains the most critical tool in the fight against malaria, with a heavy reliance on pyrethroid insecticides. However, widespread pyrethroid resistance jeopardises the effectiveness of these methods. Currently, the number of diagnostic markers available to track pyrethroid resistance in endemic settings is limited, focusing mainly on changes at the insecticide target site. Genetic analysis of seven insecticide-resistant populations from West Africa, a region with intense insecticide resistance, reveals shared loci associated with pyrethroid resistance among the sister species of the An. gambiae complex including kdr, GSTE1-8 and the CYP6P region. Notably, a mutation in the voltage-gated sodium channel, I1527T, previously identified in An. coluzzii and An. gambiae, was detected in wild-caught An. arabiensis from Burkina Faso. Additionally, a mutation, L207I, in GSTE7 common to An. coluzzii and An. arabiensis, significantly increases survivorship to deltamethrin. With the additional integration of RNAseq and data from the Anopheles gambiae 1000 genomes project, we were able to identify putative eQTLs associated with the expression of major insecticide resistance-related transcripts, such as CYP6P3, CYP9K1 and CYP6AA1. This study reveals several potential diagnostic markers of resistance that can be implemented in endemic settings and identifies putative introgression between An. arabiensis and An. coluzzii in Burkina Faso.

genetics↗

bioRxiv2025

Exposure to pyrethroid insecticides modulates immunity of Anopheles against Plasmodium falciparum

Transmission of malaria parasites relies on the blood-feeding behaviour of female Anopheles mosquitoes and can be prevented by vector control methods. Particularly, the usage of pyrethroid-containing insecticide-treated nets (ITNs) remains a cornerstone of malaria prevention. Whilst ITNs are primarily designed to induce mosquito mortality, their impact on parasite development, particularly in the context of pyrethroid resistance, is poorly understood. Our study reveals that sub-lethal pyrethroid exposure triggers systemic increases in reactive oxygen and nitrogen species reducing transmission efficacy of Plasmodium falciparum. Production of reactive nitrogen species in granulocytes induces their proliferation and primes mosquito immunity through activation of a non-canonical immune deficiency (IMD) pathway, leading to increased nitration around the midgut epithelium and subsequent ookinete destruction. These findings highlight an overlooked secondary mode of action for pyrethroids and reinforces the importance of sustained pyrethroid usage in ITNs, even in the face of high-levels of pyrethroid resistance in mosquitoes.

molecular biology↗

bioRxiv2023

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↗

bioRxiv2022

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↗

bioRxiv2022

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↗