Unraveling the miRNA Landscape in the Salivary glands and Saliva of the Tsetse Fly, Vector of African Trypanosomes
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ABSTRACT:
PROVIDER: PRJNA1216924 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR32166472_1.fastq.gz | Fastqsanger.gz | |||
| SRR32166472_2.fastq.gz | Fastqsanger.gz | |||
| SRR32166473_1.fastq.gz | Fastqsanger.gz | |||
| SRR32166473_2.fastq.gz | Fastqsanger.gz |
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Project description:MicroRNAs (miRNAs) are emerging as potential mediators of cross-species gene regulation in vector-borne diseases. In this study, we investigate miRNA presence in the tsetse fly (Glossina morsitans)-trypanosome system, focusing on salivary glands and saliva during Trypanosoma brucei infections. Using small RNA sequencing and a consensus approach combining two bioinformatics tools, miRDeep2 and sRNAtoolbox, we identified 54 unique miRNAs in tsetse saliva and salivary glands, with none originating from T. brucei. To ensure the accuracy of miRNA annotations, a robust pipeline was implemented, including de novo prediction, comparative analyses across tools, and manual curation to minimize false positives. Among the identified miRNAs, 12 were novel to tsetse flies, and 5 represented putative novel miRNAs. Salivary gland samples contained the majority of detected miRNAs, with a subset also present in saliva, with some of those saliva miRNAs exhibiting notably high relative abundance. This study demonstrates the power of integrated bioinformatics pipelines to investigate miRNAs in non-model organisms and unconventional matrices like insect saliva. Our findings contribute to the growing understanding of miRNA roles in host-vector-pathogen interactions and lay the groundwork for future functional validation studies to elucidate their biological significance.
2025-06-24 | GSE288319 | GEO
Project description:Trypanosoma brucei causes African trypanosomosis to humans and cattle, against which there are no effective vaccines or drugs. The tsetse fly Glossina morsitans morsitans is the primary vector of the species of T. brucei group. At the moment there is limited knowledge on how trypanosomes adapt to and evade the host defence responses in the salivary glands. The research described aims to identify proteins involved in the mechanisms that facilitate infection.
2016-08-08 | PXD004577 | Pride
Project description:Transcriptomic study of aging in male and female tsetse flies
| PRJEB47261 | ENA
Project description:The establishment of variant surface glycoprotein monoallelic expression revealed by single-cell RNA-seq of Trypanosoma brucei in the tsetse fly salivary glands.
| PRJEB43345 | ENA
Project description:The agents of sleeping sickness disease, Trypanosoma brucei complex parasites, are transmitted to mammalian hosts through the bite of an infected tsetse. Information on tsetse-trypanosome interactions in the salivary gland (SG) tissue, and on mammalian infective metacyclic (MC) parasites present in the SG, is sparse. We performed RNA-seq analyses from uninfected and T. b. brucei infected SGs of Glossina morsitans morsitans. Comparison of the SG transcriptomes to a whole body fly transcriptome revealed that only 2.7% of the contigs are differentially expressed during SG infection, and that only 263 contigs (0.6%) are preferentially expressed in the SGs (SG-enriched). The expression of only 37 contigs (0.08%) and 27 SG-enriched contigs (10%) were suppressed in infected SG. These suppressed contigs accounted for over 55% of the SG transcriptome, and included the most abundant putative secreted proteins with anti-hemostatic functions present in saliva. In contrast, expression of putative host proteins associated with immunity, stress, cell division and tissue remodeling were enriched in infected SG suggesting that parasite infections induce host immune and stress response(s) that likely results in tissue renewal. We also performed RNA-seq analysis from mouse blood infected with the same parasite strain, and compared the transcriptome of bloodstream form (BSF) cells with that of parasites obtained from the infected SG. Over 30% of parasite transcripts are differentially regulated between the two stages, and reflect parasite adaptations to varying host nutritional and immune ecology. These differences are associated with the switch from an amino acid based metabolism in the SG to one based on glucose utilization in the blood, and with surface coat modifications that enable parasite survival in the different hosts. This study provides a foundation on the molecular aspects of the trypanosome dialogue with its tsetse and mammalian hosts, necessary for future functional investigations.
| S-EPMC3998935 | biostudies-literature
Project description:BackgroundFor their transmission, African trypanosomes rely on their blood feeding insect vector, the tsetse fly (Glossina sp.). The ingested Trypanosoma brucei parasites have to overcome a series of barriers in the tsetse fly alimentary tract to finally develop into the infective metacyclic forms in the salivary glands that are transmitted to a mammalian host by the tsetse bite. The parasite population in the salivary gland is dense with a significant number of trypanosomes tightly attached to the epithelial cells. Our current knowledge on the impact of the infection on the salivary gland functioning is very limited. Therefore, this study aimed to gain a deeper insight into the global gene expression changes in the salivary glands of Glossina morsitans morsitans in response to an infection with the T. brucei parasite. A detailed whole transcriptome comparison of midgut-infected tsetse with and without a mature salivary gland infection was performed to study the impact of a trypanosome infection on different aspects of the salivary gland functioning and the mechanisms that are induced in this tissue to tolerate the infection i.e. to control the negative impact of the parasite presence. Moreover, a transcriptome comparison with age-matched uninfected flies was done to see whether gene expression in the salivary glands is already affected by a trypanosome infection in the tsetse midgut.ResultsBy a RNA-sequencing (RNA-seq) approach we compared the whole transcriptomes of flies with a T. brucei salivary gland/midgut infection versus flies with only a midgut infection or versus non-infected flies, all with the same age and feeding history. More than 7500 salivary gland transcripts were detected from which a core group of 1214 differentially expressed genes (768 up- and 446 down-regulated) were shared between the two transcriptional comparisons. Gene Ontology enrichment analysis and detailed gene expression comparisons showed a diverse impact at the gene transcript level. Increased expression was observed for transcripts encoding for proteins involved in immunity (like several genes of the Imd-signaling pathway, serine proteases, serpins and thioester-containing proteins), detoxification of reactive species, cell death, cytoskeleton organization, cell junction and repair. Decreased expression was observed for transcripts encoding the major secreted proteins such as 5'-nucleotidases, adenosine deaminases and the nucleic acid binding proteins Tsals. Moreover, expression of some gene categories in the salivary glands were found to be already affected by a trypanosome midgut infection, before the parasite reaches the salivary glands.ConclusionsThis study reveals that the T. brucei population in the tsetse salivary gland has a negative impact on its functioning and on the integrity of the gland epithelium. Our RNA-seq data suggest induction of a strong local tissue response in order to control the epithelial cell damage, the ROS intoxication of the cellular environment and the parasite infection, resulting in the fly tolerance to the infection. The modified expression of some gene categories in the tsetse salivary glands by a trypanosome infection at the midgut level indicate a putative anticipatory response in the salivary glands, before the parasite reaches this tissue.
| S-EPMC5123318 | biostudies-literature
Project description:Transmission of Trypanosoma brucei by tsetse flies involves the deposition of the infective quiescent metacyclic stage into the mammalian skin at the site of the fly’s bite. In the skin, the metacyclic parasites reactivate and differentiate into proliferative trypanosomes before colonizing the host's blood and tissues. We have generated an advanced human skin equivalent and used tsetse flies to naturally infect the artificial skin with trypanosomes. We have detailed the chronological order of the parasites' development in the skin and found a rapid activation and differentiation of the tsetse-transmitted cell cycle‑arrested metacyclic trypanosomes to proliferative parasites. Single-parasite transcriptomics documented the biological events during differentiation and host invasion at five different time points. After the establishment of a proliferative trypanosome population in the skin, the parasites entered a reversible quiescence program characterized by slow replication and a strongly reduced metabolism. We termed these quiescent trypanosomes skin tissue forms (STF), which may play an important role in maintaining the trypanosome infection in aparasitemic, asymptomatic individuals.
2021-05-30 | GSE174198 | GEO
Project description:The long and complex Trypanosoma brucei development in the tsetse fly vector culminates when parasites gain mammalian infectivity in the salivary glands. A key step in this process is the establishment of monoallelic variant surface glycoprotein (VSG) expression and the formation of the VSG coat. The establishment of VSG monoallelic expression is complex and poorly understood, due to the multiple parasite stages present in the salivary glands. Therefore, we sought to further our understanding of this phenomenon by performing single-cell RNA-sequencing (scRNA-seq) on these trypanosome populations. We were able to capture the developmental program of trypanosomes in the salivary glands, identifying populations of epimastigote, gamete, pre-metacyclic and metacyclic cells. Our results show that parasite metabolism is dramatically remodeled during development in the salivary glands, with a shift in transcript abundance from tricarboxylic acid metabolism to glycolytic metabolism. Analysis of VSG gene expression in pre-metacyclic and metacyclic cells revealed a dynamic VSG gene activation program. Strikingly, we found that pre-metacyclic cells contain transcripts from multiple VSG genes, which resolves to singular VSG gene expression in mature metacyclic cells. Single molecule RNA fluorescence in situ hybridisation (smRNA-FISH) of VSG gene expression following in vitro metacyclogenesis confirmed this finding. Our data demonstrate that multiple VSG genes are transcribed before a single gene is chosen. We propose a transcriptional race model governs the initiation of monoallelic expression.
| S-EPMC8509897 | biostudies-literature
Project description:Salivary glands (SG) arise from ectodermal tissue between 6 and 12th weeks of intrauterine life through finely regulated epithelial-mesenchymal interactions. For this reason, different types of structural congenital anomalies, ranging from asymptomatic anatomical variants to alterations associated with syndromic conditions, have been described. Notable glandular parenchyma anomalies are the SG aplasia and the ectopic SG tissue. Major SG aplasia is a developmental anomaly, leading to variable degrees of xerostomia, and oral dryness. Ectopic SG tissue can occur as accessory gland tissue, salivary tissue associated with branchial cleft anomalies, or true heterotopic SG tissue. Among salivary ducts anomalies, congenital atresia is a rare developmental anomaly due to duct canalization failure in oral cavity, lead to salivary retention posterior to the imperforate orifice. Accessory ducts originate from the invagination of the developing duct in two places or from the premature ventral branching of the main duct. Heterotopic ducts may arise from glandular bud positioned in an anomalous site lateral to the stomodeum or from the failure of the intraoral groove development, hindering their proximal canalization. These anomalies require multidisciplinary approach to diagnosis and treatment. While ectopic or accessory SG tissue/ducts often do not require any treatment, patients with SG aplasia could benefit from strategies for restoring SG function. This article attempts to review the literature on SG parenchyma and ducts anomalies in head and neck region providing clinicians with a comprehensive range of clinical phenotypes and possible future applications of bioengineered therapies for next-generation of regenerative medicine.
| S-EPMC6617833 | biostudies-literature
Project description:Enteric viruses like norovirus, rotavirus and astrovirus have long been accepted as spreading in the population through fecal-oral transmission: viruses are shed into feces from one host and enter the oral cavity of another, bypassing salivary glands (SGs) and reaching the intestines to replicate, be shed in feces and repeat the transmission cycle1. Yet there are viruses (for example, rabies) that infect the SGs2,3, making the oral cavity one site of replication and saliva one conduit of transmission. Here we report that enteric viruses productively and persistently infect SGs, reaching titres comparable to those in the intestines. We demonstrate that enteric viruses get released into the saliva, identifying a second route of viral transmission. This is particularly significant for infected infants, whose saliva directly transmits enteric viruses to their mothers' mammary glands through backflow during suckling. This sidesteps the conventional gut-mammary axis route4 and leads to a rapid surge in maternal milk secretory IgA antibodies5,6. Lastly, we show that SG-derived spheroids7 and cell lines8 can replicate and propagate enteric viruses, generating a scalable and manageable system of production. Collectively, our research uncovers a new transmission route for enteric viruses with implications for therapeutics, diagnostics and importantly sanitation measures to prevent spread through saliva.
| S-EPMC9243862 | biostudies-literature