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Garcia-Longoria Batanete, L.

Publications and source records attributed to Garcia-Longoria Batanete, L..

3 recordsLinked to original sources

Parasite epigenetic memory and blood barriers dictate host transcriptional responses during generalist host-shifts

The evolutionary success of generalist parasites is often attributed to their capacity to rapidly navigate divergent host environments through transcriptional plasticity. While host-parasite dynamics are frequently studied in avian models, the immunogenic impact of the heterologous blood matrix, a critical variable in cross-species inoculation experiments, is rarely accounted for. In this study, we investigated the host-transcriptomic landscape of domestic canaries (Serinus canaria) infected with the avian malaria parasite Plasmodium homocircumflexum (lineage COLL4), employing a crosswise infection design to differentiate between homologous and heterologous donor sources. By implementing a factorial experimental framework, we successfully isolated the transcriptional noise induced by the heterologous blood matrix per se, revealing that mismatched transfusions trigger significant, non-specific innate immune activation independently of parasite presence. Upon correcting for this background effect, we observed distinct transcriptional trajectories: while adapted (homologous) infections induced a metabolic catalytic overload driven by key kinase hubs (e.g., AKT1, CDK6), heterologous infections were characterized by a shift toward structural and ribosomal regulation. These divergence patterns in the host, combined with the strain-specific transcription of the parasite, suggest that early infection phases are heavily constrained by recent host-switching events. Our results demonstrate that this epigenetic memory acts as a fundamental determinant of virulence, providing a new systems-based framework for understanding how pathogen history and host-donor compatibility reshape infection dynamics and host molecular outcomes during the colonization of novel ecological frontiers.

evolutionary biology↗

Generalist malaria parasites and host imprinting: Unveiling transcriptional memory

Generalist parasites must rapidly adapt to diverse host environments to ensure their survival and transmission. Parasites may employ fixed genetic responses, transcriptional plasticity, or epigenetic mechanisms to optimize survival. The avian malaria parasite Plasmodium homocircumflexum serves as an ideal model for studying transcriptional variation and adaptive strategies. We experimentally inoculated P. homocircumflexum into different bird hosts, bypassing vector recombination, to investigate whether parasite gene expression remains stable across hosts, resets in response to new environments, or reflects epigenetic inheritance. Our study evaluates four potential mechanisms: (1) A universal gene expression profile ("one key fits all"), where expression remains stable across hosts. Our outcomes revealed that gene expression differed significantly depending on the host species and time post-infection, thus rejecting this hypothesis. (2) Complete transcriptional plasticity, where gene expression is fully determined by the recipient host. Contrary to this hypothesis, we observed that gene expression was primarily influenced by the donor at 8 days post-infection (dpi), whereas gene expression was more aligned with the recipient host at 16 dpi. (3) Epigenetic inheritance, where early-stage gene expression reflects the donor host but gradually adjusts to the recipient. Our results support this mechanism, as 2,647 differentially expressed genes (DEGs) were associated with donors at 8 dpi, whereas 271 DEGs were linked to the recipient by 16 dpi. (4) Selection-driven differentiation favoring specific haplotypes. This latter hypothesis was not supported since SNP analyses showed low genetic differentiation. These findings suggest a P. homocircumflexum transition from donor-dependent to recipient-dependent gene expression, likely mediated by epigenetic regulation and transcriptional plasticity.

genomics↗

Immune gene expression in the mosquito vector Culex quinquefasciatus during an avian malaria infection

Plasmodium relictum is the most widespread avian malaria parasite in the world. It is listed as one of the 100 most dangerous invasive species, having been responsible for the extinction of several endemic bird species, and the near-demise of several others. Here we present the first transcriptomic study examining the effect of P. relictum on the immune system of its vector (the mosquito Culex quinquefasciatus) at different times post-infection. We show that over 50% of immune genes identified as being part of the Toll pathway and 30-40% of the immune genes identified within the Imd pathway are overexpressed during the critical period spanning the parasites oocyst and sporozoite formation (8-12 days), revealing the crucial role played by both these pathways in this natural mosquito-Plasmodium combination. Comparison of infected mosquitoes with their uninfected counterparts also revealed some unexpected RNA expression patterns earlier and later in the infection: Significant differences in expression of several immune effectors were observed as early as 30 minutes after the ingestion of the infected blood meal. In addition, in the later stages of the infection (towards the end of the mosquito lifespan), we observed an unexpected increase in immune investment in uninfected, but not in infected, mosquitoes. In conclusion, our work extends the comparative transcriptomic analyses of malaria-infected mosquitoes beyond human and rodent parasites and provides insights into the degree of conservation of immune pathways and into the selective pressures exerted by Plasmodium parasites on their vectors.

evolutionary biology↗