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ABSTRACT Herbivorous insects tolerate chemical and metabolic variation in their host plant diet by modulating physiological traits. Insect immune response is one such trait that plays a crucial role in maintaining fitness but can be heavily influenced by variation in host plant quality. An important question is how the use of different host plants affects the ability of herbivorous insects to resist viral pathogens. Furthermore, the transcriptional changes associated with this interaction of diet and viral pathogens remain understudied. The Melissa blue butterfly (Lycaeides melissa) has colonised the exotic legumeMedicago sativaas a larval host within the past 200 years. We used this system to study the interplay between the effects of host plant variation and viral infection on physiological responses and global gene expression. We measured immune strength in response to infection by the Junonia coenia densovirus (JcDV) in two ways: (1) direct measurement of phenoloxidase activity and melanisation, and (2) transcriptional sequencing of individuals exposed to different viral and host plant treatments. Our results demonstrate that viral infection caused total phenoloxidase (total PO) to increase and viral infection and host plant interactively affected total PO such that for infected larvae, total PO was significantly higher for larvae consuming the native host plant. Additionally,L. melissalarvae differentially expressed several hundred genes in response to host plant treatment, but with minimal changes in gene expression in response to viral infection. Not only immune genes, but several detoxification, transporter, and oxidase genes were differentially expressed in response to host plant treatments. These results demonstrate that in herbivorous insects, consumption of a novel host plant can alter both physiological and transcriptional responses relevant to viral infection, emphasising the importance of considering immune and detoxification mechanisms into models of evolution of host range in herbivorous insects. 

Streptococcus sinensis is a recently identified member of the Mitis group of streptococci. This species has been associated with infective endocarditis; however its mechanisms of pathogenesis and virulence are not fully understood. This study aimed to investigate the influence of the competence-stimulating peptide (CSP) and the competence regulon quorum-sensing circuitry (ComABCDE) on subsequent gene transcription and expression, as well as resultant phenotypes. In this study we confirmed the native CSP identity, ascertained when endogenous CSP was produced and completed a transcriptome-wide analysis of all genes following CSP exposure. RNA sequencing analysis revealed the upregulation of genes known to be associated with competence, biofilm formation and virulence. As such, a variety of phenotypic assays were utilized to assess the correlation between increased mRNA expression and potential phenotype response, ultimately gaining insight into the effects of CSP on both gene expression and developed phenotypes. The results indicated that the addition of exogenous CSP aided in competence development and successful transformation, yielding an average transformation efficiency comparable to that of other Mitis group streptococci. Additional studies are needed to further delineate the effects of CSP exposure on biofilm formation and virulence. Overall, this study provides novel information regarding S. sinensis and provides a substantial foundation on which this species and its role in disease pathogenesis can be further investigated. 

The 3′ untranslated regions (3′ UTRs) of mRNAs serve as hubs for post-transcriptional control as the targets of microRNAs (miRNAs) and RNA-binding proteins (RBPs). Sequences in 3′ UTRs confer alterations in mRNA stability, direct mRNA localization to subcellular regions, and impart translational control. Thousands of mRNAs are localized to subcellular compartments in neurons—including axons, dendrites, and synapses—where they are thought to undergo local translation. Despite an established role for 3′ UTR sequences in imparting mRNA localization in neurons, the specific RNA sequences and structural features at play remain poorly understood. The nervous system selectively expresses longer 3′ UTR isoforms via alternative polyadenylation (APA). The regulation of APA in neurons and the neuronal functions of longer 3′ UTR mRNA isoforms are starting to be uncovered. Surprising roles for 3′ UTRs are emerging beyond the regulation of protein synthesis and include roles as RBP delivery scaffolds and regulators of alternative splicing. Evidence is also emerging that 3′ UTRs can be cleaved, leading to stable, isolated 3′ UTR fragments which are of unknown function. Mutations in 3′ UTRs are implicated in several neurological disorders—more studies are needed to uncover how these mutations impact gene regulation and what is their relationship to disease severity.