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ABSTRACT The protein disulfide isomerase (PDI) family is a group of enzymes that have thiol-disulfide oxidoreductase, disulfide isomerase, and redox-dependent chaperone activities. PDIs facilitate diverse infections in mammalian hosts by directly binding to pathogens, immunomodulation, or enabling microbial invasion of host cells. PDI homologs within pathogens are also potential virulence factors. However, whether PDIs within blood-feeding ticks influence microbial infection remains unknown. In this study, we investigated the role of Ixodes scapularis PDIs, on the Lyme disease agent, Borrelia burgdorferi. I. scapularis has five PDIs (IsPDIs), and IsPDIA6 gene expression is reduced upon B. burgdorferi infection in the tick. IsPDIA6-mediated trypsin inhibitor gene expression contributes to B. burgdorferi colonization within the tick midgut. IsPDIA6 is also secreted into the host during tick feeding, alters cytokine/chemokine expression at the tick bite site, and influences the initial stage of bacterial infection in mice. These data demonstrate that a PDI from a blood-feeding vector plays a role in the life cycle of an extracellular pathogen.IMPORTANCEVector-borne diseases are a leading cause of death and illness worldwide, and more than 80% of the global population live in areas at risk from at least one major vector-borne disease. In this study, we demonstrate a dual role of a specific Ixodes tick protein disulfide isomerase (PDI) in inhibiting the ability of the Lyme disease agent to colonize ticks and also in enhancing the initial stage of spirochete infection of mice. This study represents a novel conceptual advancement that a PDI from a blood-feeding vector plays important roles in the life cycle of an extracellular pathogen.

Abstract Gene-edited mosquitoes lacking a gamma-interferon-inducible lysosomal thiol reductase-like protein, namely (mosGILT null ) have lower Plasmodium infection, which is linked to impaired ovarian development and immune activation. The transcriptome of mosGILT null Anopheles gambiae was therefore compared to wild type (WT) mosquitoes by RNA-sequencing to delineate mosGILT-dependent pathways. Compared to WT mosquitoes, mosGILT null A. gambiae demonstrated altered expression of genes related to oogenesis, 20-hydroxyecdysone synthesis, as well as immune-related genes. Serendipitously, the zero population growth gene, zpg, an essential regulator of germ cell development was found to be one of the most downregulated genes in mosGILT null mosquitoes. These results provide a crucial missing link between two previous studies on the role of zpg and mosGILT in ovarian development. This study further demonstrates that mosGILT has the potential to serve as a target for the biological control of mosquito vectors and to influence the Plasmodium life cycle within the vector.

Tillage practices significantly influence crop yield and soil quality. This study investigated the impact of rotary tillage (RT) and deep tillage (DT) on soil properties, microbial diversity, and melon (Cucumis melo L.) root growth and yield. RT involved breaking up the topsoil to a depth of 15 cm using a rotary tiller, while DT employed a rotary tiller followed by a moldboard plow to turn the soil layer over to a depth of 35 cm. The melon variety “Nasimi” was used as the material. Our findings revealed a remarkable response of soil phosphorus to tillage practices. High-throughput sequencing results revealed a significant impact of tillage practices on the soil fungal composition, richness, and diversity but little impact on the bacterial communities. Compared to RT, DT markedly enhanced melon root length, root surface area, root volume, and mean root diameter by 47.42%, 56.70%, 58.83%, and 27.28%, respectively. Additionally, DT treatments significantly increased melon yield (53.46%) compared to RT. The results indicate that DT improves soil nutrient availability, affects soil fungal community characteristics, and optimizes root distribution in soil, thereby improving melon yield. The findings offer valuable theoretical insights for the implementation of effective tillage practices in open-field melon cultivation.

ABSTRACTWhen a female mosquito engorges on a mammalian host, components of the blood meal can affect mosquito fitness and indirectly influence pathogen infectivity. We demonstrate that mammalian adiponectin, ingested during Anopheles gambiae blood feeding, co-localizes within mosquito midguts and decreases Plasmodium infection in the vector. Transcriptomic and RNAi studies reveal that the A. gambiae adiponectin receptor is involved in downregulating lipophorin, a lipid transporter that is important for egg development and Plasmodium infection in mosquitoes. These studies characterize a cross-phyla interaction between the mammalian host and A. gambiae that negatively impacts Plasmodium survival in its arthropod vector.IMPORTANCEWhen a female mosquito takes a blood meal from a mammalian host, components of the blood meal can affect mosquito fitness and indirectly influence pathogen infectivity. We identified a pathway involving an Anopheles gambiae adiponectin receptor, which, triggered by adiponectin from an incoming blood meal, decreases Plasmodium infection in the mosquito. Activation of this pathway negatively regulates lipophorin expression, an important lipid transporter that both enhances egg development and Plasmodium infection. This is an unrecognized cross-phyla interaction between a mosquito and its vertebrate host. These processes are critical to understanding the complex life cycle of mosquitoes and Plasmodium following a blood meal and may be applicable to other hematophagous arthropods and vector-borne infectious agents.

Guinea pigs repeatedly exposed to Ixodes scapularis develop acquired resistance to the ticks (ATR). The molecular mechanisms of ATR have not been fully elucidated, and partially involves immune responses to proteins in tick saliva. In this study, we examined the metabolome of sera of guinea pigs during the development of ATR. Induction of components of the tyrosine metabolic pathway, including hydroxyphenyllactic acid (HPLA), were associated with ATR. We therefore administered HPLA to mice, an animal that does not develop ATR, and exposed the animals to I. scapularis. We also administered nitisinone, a known inhibitor of tyrosine degradation, to another group of mice. The mortality of I. scapularis that fed on mice given HPLA or nitisinone was 26 % and 72 % respectively, compared with 2 % mortality among ticks that fed on control animals. These data indicate that tick bites alter the guinea pig metabolome, and that the tyrosine metabolism pathway can potentially be targeted for I. scapularis control.