scholarly journals A genome-wide screening for RNAi pathway proteins in Acari

2020 ◽  
Author(s):  
Beatrice T Nganso ◽  
Noa Sela ◽  
Victoria Soroker
Keyword(s):  
Gene Silencing ◽  
Micro Rna ◽  
Rnai Pathway ◽  
Comparative Genomic ◽  
Specific Gene ◽  
C Elegans ◽  
Conserved Sequence ◽  
A Genome ◽  
Systemic Rnai ◽  
Amplification Mechanism

Abstract Background RNA interference (RNAi) is a highly conserved, sequence-specific gene silencing mechanism present in Eukaryotes. Three RNAi pathways critical for organismal development and survival are known, namely micro-RNA (miRNA), Piwi-interacting RNA (piRNA) and short interfering RNA (siRNA) pathways. Little knowledge exist about the genes involved in these pathways in Acari. Moreover, variable successes has been obtained in gene knockdown via siRNA pathway in functional genomics and management of Acari species. We hypothesized that the clue may be in the variability in the composition and the efficacy of siRNAi machinery among Acari. Results Both comparative genomic analyses and domain annotation suggest that all the analyzed species have orthologs of genes that mediate gene silencing via the three RNAi pathways though gene duplication and/or loss have occurred in the different species. We also identified orthologs of Caenorhabditis elegans RNA-dependent RNA polymerase (RdRP) gene in all Acari species though no secondary Argonaute homologs that operate with this gene in siRNA amplification mechanism were found. This finding suggests that the siRNA amplification mechanism present in Acari may be distinct from that described in C. elegans . Moreover, the genomes of these Acari species encode no ortholog of C. elegans systemic RNAi defective 1 (Sid-1) that mediate systemic RNAi, suggesting that the phenomena of systemic and parental RNAi that has been reported in some Acari species probably occur through a different mechanism. Orthologs of RNAi spreading defective-3 (Rsd-3) gene and scavenger receptors namely Eater and SR-CI that mediate endocytosis cellular update of dsRNA in C. elegans and Drosophila melanogaster were found in Acari genomes. This result suggests that cellular dsRNA uptake in Acari is endocytosis-dependent. Detailed phylogenetic analyses of core RNAi pathway genes in the studied Acari species revealed that their evolution is compatible with the proposed monophyletic evolution of this group. Conclusions Taken together, our in silico comparative analyses have revealed the potential activity of all three pathways in Acari. However, much experimental work remains to be done in elucidating the operating mechanisms behind these pathways in particular those that govern systemic/parental RNAi and siRNA amplification in Acari.

scholarly journals A genome-wide screening for RNAi pathway genes in Acari

2020 ◽  
Author(s):  
Victoria Soroker ◽  
Beatrice T Nganso ◽  
Noa Sela
Keyword(s):  
Gene Silencing ◽  
Micro Rna ◽  
Rnai Pathway ◽  
Comparative Genomic ◽  
Specific Gene ◽  
C Elegans ◽  
Conserved Sequence ◽  
A Genome ◽  
Systemic Rnai ◽  
Amplification Mechanism

Abstract BackgroundRNA interference (RNAi) is a highly conserved, sequence-specific gene silencing mechanism present in Eukaryotes. Three RNAi pathways critical for organismal development and survival are known, namely micro-RNA (miRNA), Piwi-interacting RNA (piRNA) and short interfering RNA (siRNA) pathways. Little knowledge exist about the genes involved in these pathways in Acari. Moreover, variable successes has been obtained in gene knockdown via siRNA pathway in functional genomics and management of Acari species. We hypothesized that the clue may be in the variability in the composition and the efficacy of siRNAi machinery among Acari. ResultsBoth comparative genomic analyses and domain annotation suggest that all the analyzed species have orthologs of genes that mediate gene silencing via the three RNAi pathways though gene duplication and/or loss have occurred in the different species. We also identified orthologs of Caenorhabditis elegans RNA-dependent RNA polymerase (RdRP) gene in all Acari species though no secondary Argonaute homologs that operate with this gene in siRNA amplification mechanism were found. This finding suggests that the siRNA amplification mechanism present in Acari may be distinct from that described in C. elegans. Moreover, the genomes of these Acari species encode no ortholog of C. elegans systemic RNAi defective 1 (Sid-1) that mediate systemic RNAi, suggesting that the phenomena of systemic and parental RNAi that has been reported in some Acari species probably occur through a different mechanism. Orthologs of RNAi spreading defective-3 (Rsd-3) gene and scavenger receptors namely Eater and SR-CI that mediate endocytosis cellular update of dsRNA in C. elegans and Drosophila melanogaster were found in Acari genomes. This result suggests that cellular dsRNA uptake in Acari is endocytosis-dependent. Detailed phylogenetic analyses of core RNAi pathway genes in the studied Acari species revealed that their evolution is compatible with the proposed monophyletic evolution of this group.ConclusionsTaken together, our in silico comparative analyses have revealed the potential activity of all three pathways in Acari. However, much experimental work remains to be done in elucidating the operating mechanisms behind these pathways in particular those that govern systemic/parental RNAi and siRNA amplification in Acari.

scholarly journals A genome-wide screening for RNAi pathway proteins in Acari

2020 ◽  
Author(s):  
Beatrice T Nganso ◽  
Noa Sela ◽  
Victoria Soroker
Keyword(s):  
Micro Rna ◽  
Rnai Pathway ◽  
Comparative Genomic ◽  
Specific Gene ◽  
C Elegans ◽  
Conserved Sequence ◽  
Core Proteins ◽  
A Genome ◽  
Systemic Rnai ◽  
Amplification Mechanism

Abstract Background: RNA interference (RNAi) is a highly conserved, sequence-specific gene silencing mechanism present in Eukaryotes. Three RNAi pathways are known, namely micro-RNA (miRNA), piwi-interacting RNA (piRNA) and short interfering RNA (siRNA). However, little knowledge exists about the proteins involved in these pathways in Acari. Moreover, variable successes has been obtained in gene knockdown via siRNA pathway in their functional genomics and management. We hypothesized that the clue may be in the variability of the composition and the efficacy of siRNA machinery among Acari.Results: Both comparative genomic analyses and domain annotation suggest that all the analyzed species have homologs of putative core proteins that mediate cleaving of targeted genes via the three RNAi pathways. We identified putative homologs of Caenorhabditis elegans RNA-dependent RNA polymerase (RdRP) protein in all species though no secondary Argonaute homologs that operate with this protein in siRNA amplification mechanism were found, suggesting that the siRNA amplification mechanism present in Acari may be distinct from that described in C. elegans. Moreover, the genomes of these species do not encode homologs of C. elegans systemic RNAi defective-1 (Sid-1) protein that mediate silencing of the mRNA target throughout the treated organisms suggesting that the phenomena of systemic RNAi that has been reported in some Acari species probably occur through a different mechanism. However, homologs of putative RNAi spreading defective-3 (Rsd-3) protein and scavenger receptors namely Eater and SR-CI that mediate endocytosis cellular update of dsRNA in C. elegans and Drosophila melanogaster were found in Acari genomes. This result suggests that cellular dsRNA uptake in Acari is endocytosis-dependent. Detailed phylogenetic analyses of core RNAi pathway proteins in the studied species revealed that their evolution is compatible with the proposed monophyletic evolution of this group.Conclusions: Our analyses have revealed the potential activity of all three pathways in Acari. Still, much experimental work remains to be done to confirm the mechanisms behind these pathways in particular those that govern systemic/parental RNAi and siRNA amplification in Acari. Disclosure of these mechanisms will facilitate the development of new and specific management tools for the harmful species and enrichment of the beneficial species.

scholarly journals A genome-wide screening for RNAi pathway proteins in Acari

BMC Genomics ◽  
2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Beatrice T. Nganso ◽  
Noa Sela ◽  
Victoria Soroker
Keyword(s):  
Micro Rna ◽  
Rnai Pathway ◽  
Comparative Genomic ◽  
Specific Gene ◽  
C Elegans ◽  
Conserved Sequence ◽  
Core Proteins ◽  
A Genome ◽  
Systemic Rnai ◽  
Amplification Mechanism

Abstract Background RNA interference (RNAi) is a highly conserved, sequence-specific gene silencing mechanism present in Eukaryotes. Three RNAi pathways are known, namely micro-RNA (miRNA), piwi-interacting RNA (piRNA) and short interfering RNA (siRNA). However, little knowledge exists about the proteins involved in these pathways in Acari. Moreover, variable successes has been obtained in gene knockdown via siRNA pathway in their functional genomics and management. We hypothesized that the clue may be in the variability of the composition and the efficacy of siRNA machinery among Acari. Results Both comparative genomic analyses and domain annotation suggest that all the analyzed species have homologs of putative core proteins that mediate cleaving of targeted genes via the three RNAi pathways. We identified putative homologs of Caenorhabditis elegans RNA-dependent RNA polymerase (RdRP) protein in all species though no secondary Argonaute homologs that operate with this protein in siRNA amplification mechanism were found, suggesting that the siRNA amplification mechanism present in Acari may be distinct from that described in C. elegans. Moreover, the genomes of these species do not encode homologs of C. elegans systemic RNAi defective-1 (Sid-1) protein that mediate silencing of the mRNA target throughout the treated organisms suggesting that the phenomena of systemic RNAi that has been reported in some Acari species probably occur through a different mechanism. However, homologs of putative RNAi spreading defective-3 (Rsd-3) protein and scavenger receptors namely Eater and SR-CI that mediate endocytosis cellular update of dsRNA in C. elegans and Drosophila melanogaster were found in Acari genomes. This result suggests that cellular dsRNA uptake in Acari is endocytosis-dependent. Detailed phylogenetic analyses of core RNAi pathway proteins in the studied species revealed that their evolution is compatible with the proposed monophyletic evolution of this group. Conclusions Our analyses have revealed the potential activity of all three pathways in Acari. Still, much experimental work remains to be done to confirm the mechanisms behind these pathways in particular those that govern systemic/parental RNAi and siRNA amplification in Acari. Disclosure of these mechanisms will facilitate the development of new and specific management tools for the harmful species and enrichment of the beneficial species.

scholarly journals A genome-wide screening for RNAi pathway proteins in Acari

2020 ◽  
Author(s):  
Beatrice T Nganso ◽  
Noa Sela ◽  
Victoria Soroker
Keyword(s):  
Micro Rna ◽  
Rnai Pathway ◽  
Comparative Genomic ◽  
Specific Gene ◽  
C Elegans ◽  
Conserved Sequence ◽  
Core Proteins ◽  
A Genome ◽  
Systemic Rnai ◽  
Amplification Mechanism

Abstract BackgroundRNA interference (RNAi) is a highly conserved, sequence-specific gene silencing mechanism present in Eukaryotes. Three RNAi pathways are known, namely micro-RNA (miRNA), Piwi-interacting RNA (piRNA) and short interfering RNA (siRNA). However, little knowledge exists about the proteins involved in these pathways in Acari. Moreover, variable successes has been obtained in gene knockdown via siRNA pathway in their functional genomics and management. We hypothesized that the clue may be in the variability of the composition and the efficacy of siRNA machinery among Acari.ResultsBoth comparative genomic analyses and domain annotation suggest that all the analyzed species have homologs of putative core proteins that mediate cleaving of targeted genes via the three RNAi pathways. We identified putative homologs of Caenorhabditis elegans RNA-dependent RNA polymerase (RdRP) protein in all species though no secondary Argonaute homologs that operate with this protein in siRNA amplification mechanism were found, suggesting that the siRNA amplification mechanism present in Acari may be distinct from that described in C. elegans. Moreover, the genomes of these species do not encode homologs of C. elegans systemic RNAi defective 1 (Sid-1) protein that mediate silencing of the mRNA target throughout the treated organisms suggesting that the phenomena of systemic RNAi that has been reported in some Acari species probably occur through a different mechanism. However, Homologs of putative RNAi spreading defective-3 (Rsd-3) protein and scavenger receptors namely Eater and SR-CI that mediate endocytosis cellular update of dsRNA in C. elegans and Drosophila melanogaster were found in Acari genomes. This result suggests that cellular dsRNA uptake in Acari is endocytosis-dependent. Detailed phylogenetic analyses of core RNAi pathway proteins in the studied species revealed that their evolution is compatible with the proposed monophyletic evolution of this group.ConclusionsOur analyses have revealed the potential activity of all three pathways in Acari. Still, much experimental work remains to be done to confirm the mechanisms behind these pathways in particular those that govern systemic/parental RNAi and siRNA amplification in Acari. Disclosure of these mechanisms will facilitate the development of new and specific management tools for the harmful species and enrichment of the beneficial species.

scholarly journals A deletion polymorphism in the Caenorhabditis elegans RIG-I homolog disables viral RNA dicing and antiviral immunity

eLife ◽  
2013 ◽  
Vol 2 ◽  
Author(s):  
Alyson Ashe ◽  
Tony Bélicard ◽  
Jérémie Le Pen ◽  
Peter Sarkies ◽  
Lise Frézal ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Genome Wide Association Study ◽  
Rna Virus ◽  
Rnai Pathway ◽  
Animal Cells ◽  
C Elegans ◽  
Base Pair Deletion ◽  
A Genome ◽  
Positive Strand Rna ◽  
Viral Recognition

RNA interference defends against viral infection in plant and animal cells. The nematode Caenorhabditis elegans and its natural pathogen, the positive-strand RNA virus Orsay, have recently emerged as a new animal model of host-virus interaction. Using a genome-wide association study in C. elegans wild populations and quantitative trait locus mapping, we identify a 159 base-pair deletion in the conserved drh-1 gene (encoding a RIG-I-like helicase) as a major determinant of viral sensitivity. We show that DRH-1 is required for the initiation of an antiviral RNAi pathway and the generation of virus-derived siRNAs (viRNAs). In mammals, RIG-I-domain containing proteins trigger an interferon-based innate immunity pathway in response to RNA virus infection. Our work in C. elegans demonstrates that the RIG-I domain has an ancient role in viral recognition. We propose that RIG-I acts as modular viral recognition factor that couples viral recognition to different effector pathways including RNAi and interferon responses.

scholarly journals Maternal and zygotic gene regulatory effects of endogenous RNAi pathways

2018 ◽  
Author(s):  
Miguel Vasconcelos Almeida ◽  
António Miguel de Jesus Domingues ◽  
René F. Ketting
Keyword(s):  
Gene Expression ◽  
Caenorhabditis Elegans ◽  
Gene Silencing ◽  
Small Rnas ◽  
Self Regulation ◽  
Fine Tuning ◽  
Specific Gene ◽  
Next Generation ◽  
C Elegans ◽  
Argonaute Proteins

AbstractEndogenous small RNAs (sRNAs) and Argonaute proteins are ubiquitous regulators of gene expression in germline and somatic tissues. sRNA-Argonaute complexes are often expressed in gametes and are consequently inherited by the next generation upon fertilization. In Caenorhabditis elegans, 26G-RNAs are primary endogenous sRNAs that trigger the expression of downstream secondary sRNAs. Two subpopulations of 26G-RNAs exist, each of which displaying strongly compartmentalized expression: one is expressed in the spermatogenic gonad and associates with the Argonautes ALG-3/4; plus another expressed in oocytes and in embryos, which associates with the Argonaute ERGO-1. The determinants and dynamics of gene silencing elicited by 26G-RNAs are largely unknown. Here, we provide diverse new insights into these endogenous sRNA pathways of C. elegans. Using genetics and deep sequencing, we dissect a maternal effect of the ERGO-1 branch sRNA pathway. We find that maternal primary sRNAs can trigger the production of zygotic secondary sRNAs that are able to silence targets, even in the absence of zygotic primary triggers. Thus, the interaction of maternal and zygotic sRNA populations, assures target gene silencing throughout animal development. Furthermore, we find that sRNA abundance, the pattern of origin of sRNA and 3’ UTR length are predictors of the regulatory outcome by the Argonautes ALG-3/4. Lastly, we discovered that ALG-3- and ALG-4-bound 26G-RNAs are dampening the expression of their own mRNAs, revealing a negative feedback loop. Altogether, we provide several new regulatory insights on the dynamics, target regulation and self-regulation of the endogenous RNAi pathways of C. elegans.Author SummarySmall RNAs (sRNAs) and their partner Argonaute proteins regulate the expression of target RNAs. When sperm and egg meet upon fertilization, a diverse set of proteins and RNA, including sRNA-Argonaute complexes, is passed on to the developing progeny. Thus, these two players are important to initiate specific gene expression programs in the next generation. The nematode Caenorhabditis elegans expresses several classes of sRNAs. 26G-RNAs are a particular class of sRNAs that are divided into two subpopulations: one expressed in the spermatogenic gonad and another expressed in oocytes and in embryos. In this work, we describe the dynamics whereby oogenic 26G-RNAs setup gene silencing in the next generation. We also show several ways that spermatogenic 26G-RNAs and their partner Argonautes, ALG-3 and ALG-4, use to regulate their targets. Finally, we show that ALG-3 and ALG-4 are fine-tuning their own expression, a rare role of Argonaute proteins. Overall, we provide new insights into how sRNAs and Argonautes are regulating gene expression.

scholarly journals Pseudomonas donghuensis HYS gtrA/B/II Gene Cluster Contributes to Its Pathogenicity toward Caenorhabditis elegans

2021 ◽  
Vol 22 (19) ◽  
pp. 10741
Author(s):  
Yaqian Xiao ◽  
Panning Wang ◽  
Xuesi Zhu ◽  
Zhixiong Xie
Keyword(s):  
Caenorhabditis Elegans ◽  
Gene Cluster ◽  
Mapk Pathway ◽  
Genomic Analysis ◽  
Virulence Gene ◽  
Comparative Genomic ◽  
Specific Gene ◽  
C Elegans ◽  
O Antigen ◽  
Specific Virulence

Pseudomonas donghuensis HYS is more virulent than P. aeruginosa toward Caenorhabditis elegans but the mechanism underlying virulence is unclear. This study is the first to report that the specific gene cluster gtrA/B/II in P. donghuensis HYS is involved in the virulence of this strain toward C. elegans, and there are no reports of GtrA, GtrB and GtrII in any Pseudomonas species. The pathogenicity of P. donghuensis HYS was evaluated using C. elegans as a host. Based on the prediction of virulence factors and comparative genomic analysis of P. donghuensis HYS, we identified 42 specific virulence genes in P. donghuensis HYS. Slow-killing assays of these genes showed that the gtrAB mutation had the greatest effect on the virulence of P. donghuensis HYS, and GtrA, GtrB and GtrII all positively affected P. donghuensis HYS virulence. Two critical GtrII residues (Glu47 and Lys480) were identified in P. donghuensis HYS. Transmission electron microscopy (TEM) showed that GtrA, GtrB and GtrII were involved in the glucosylation of lipopolysaccharide (LPS) O-antigen in P. donghuensis HYS. Furthermore, colony-forming unit (CFU) assays showed that GtrA, GtrB and GtrII significantly enhanced P. donghuensis HYS colonization in the gut of C. elegans, and glucosylation of LPS O-antigen and colonization in the host intestine contributed to the pathogenicity of P. donghuensis HYS. In addition, experiments using the worm mutants ZD101, KU4 and KU25 revealed a correlation between P. donghuensis HYS virulence and the TIR-1/SEK-1/PMK-1 pathways of the innate immune p38 MAPK pathway in C. elegans. In conclusion, these results reveal that the specific virulence gene cluster gtrA/B/II contributes to the unique pathogenicity of HYS compared with other pathogenic Pseudomonas, and that this process also involves C. elegans innate immunity. These findings significantly increase the available information about GtrA/GtrB/GtrII-based virulence mechanisms in the genus Pseudomonas.

scholarly journals How to make a rodent giant: Genomic basis and tradeoffs of gigantism in the capybara, the world’s largest rodent

2020 ◽  
Author(s):  
Santiago Herrera-Álvarez ◽  
Elinor Karlsson ◽  
Oliver A Ryder ◽  
Kerstin Lindblad-Toh ◽  
Andrew J Crawford
Keyword(s):  
Body Size ◽  
Draft Genome ◽  
Large Body ◽  
Comparative Genomic ◽  
Specific Gene ◽  
Large Body Size ◽  
Synonymous Mutations ◽  
Intragenomic Conflict ◽  
Genome Wide ◽  
A Genome

Abstract Gigantism results when one lineage within a clade evolves extremely large body size relative to its small-bodied ancestors, a common phenomenon in animals. Theory predicts that the evolution of giants should be constrained by two tradeoffs. First, because body size is negatively correlated with population size, purifying selection is expected to be less efficient in species of large body size, leading to increased mutational load. Second, gigantism is achieved through generating a higher number of cells along with higher rates of cell proliferation, thus increasing the likelihood of cancer. To explore the genetic basis of gigantism in rodents and uncover genomic signatures of gigantism-related tradeoffs, we assembled a draft genome of the capybara (Hydrochoerus hydrochaeris), the world’s largest living rodent. We found that the genome-wide ratio of non-synonymous to synonymous mutations (ω) is elevated in the capybara relative to other rodents, likely caused by a generation-time effect and consistent with a nearly-neutral model of molecular evolution. A genome-wide scan for adaptive protein evolution in the capybara highlighted several genes controlling post-natal bone growth regulation and musculoskeletal development, which are relevant to anatomical and developmental modifications for an increase in overall body size. Capybara-specific gene-family expansions included a putative novel anticancer adaptation that involves T cell-mediated tumor suppression, offering a potential resolution to the increased cancer risk in this lineage. Our comparative genomic results uncovered the signature of an intragenomic conflict where the evolution of gigantism in the capybara involved selection on genes and pathways that are directly linked to cancer.

scholarly journals A Double-Stranded-RNA Response Program Important for RNA Interference Efficiency

2007 ◽  
Vol 27 (11) ◽  
pp. 3995-4005 ◽  
Author(s):  
Swati Choudhary ◽  
Heng-Chi Lee ◽  
Mekhala Maiti ◽  
Qun He ◽  
Ping Cheng ◽  
...  
Keyword(s):  
Rna Interference ◽  
Gene Silencing ◽  
Interferon Response ◽  
Rnai Pathway ◽  
Double Stranded Rna ◽  
Interferon Stimulated Genes ◽  
A Genome ◽  
Genome Wide Search ◽  
Host Defense Response ◽  
Optimal Function

ABSTRACT When recognized by the RNA interference (RNAi) pathway, double-stranded RNA (dsRNA) produced in eukaryotic cells results in posttranscriptional gene silencing. In addition, dsRNA can trigger the interferon response as part of the immune response in vertebrates. In this study, we show that dsRNA, but not short interfering RNA (siRNA), induces the expression of qde-2 (an Argonaute gene) and dcl-2 (a Dicer gene), two central components of the RNAi pathway in the filamentous fungus Neurospora crassa. The induction of QDE-2 by dsRNA is required for normal gene silencing, indicating that this is a regulatory mechanism that allows the optimal function of the RNAi pathway. In addition, we demonstrate that Dicer proteins (DCLs) regulate QDE-2 posttranscriptionally, suggesting a role for DCLs or siRNA in QDE-2 accumulation. Finally, a genome-wide search revealed that additional RNAi components and homologs of antiviral and interferon-stimulated genes are also dsRNA-activated genes in Neurospora. Together, our results suggest that the activation of the RNAi components is part of a broad ancient host defense response against viral and transposon infections.

scholarly journals RNAi gene knockdown in the poultry red mite, Dermanyssus gallinae (De Geer 1778), a tool for functional genomics

2020 ◽  
Author(s):  
Wan Chen ◽  
Kathryn Bartley ◽  
Francesca Nunn ◽  
Alan S. Bowman ◽  
Jeremy M. Sternberg ◽  
...  
Keyword(s):  
Gene Silencing ◽  
Oral Delivery ◽  
Egg Laying ◽  
Micro Rna ◽  
Gene Knockdown ◽  
Model Organisms ◽  
Economic Losses ◽  
Dermanyssus Gallinae ◽  
Rnai Pathway ◽  
Poultry Red Mite

Background: The avian haematophagous ectoparasite, Dermanyssus gallinae or the poultry red mite, causes significant economic losses to the egg laying industry worldwide and also represents a significant welfare threat. Current acaricide-based controls are unsustainable due to the mite's ability to rapidly develop resistance, thus developing a novel sustainable means of control for D. gallinae is a priority. RNA interference (RNAi) mediated gene silencing is a valuable tool for studying gene function in non-model organisms, but is also emerging as a novel tool for parasite control.Methods: Here we use an in silico approach to identify core RNAi pathway genes in the recently sequenced D. gallinae genome. In addition we utilise an in vitro feeding device to deliver dsRNA to D. gallinae targeting the D. gallinae vATPase subunit A (Dg vATPase A) gene and monitor gene knockdown using quantitive PCR (qPCR). Results: We identified core components of the small interfering RNA (siRNA) and micro RNA (miRNA) pathways in D. gallinae, which indicate these gene silencing pathways are likely functional. Strikingly, the Piwi-interacting RNA (piRNA) pathway was absent in D. gallinae. In addition, we demonstrate that feeding Dg vATPase A dsRNA to adult female D. gallinae results in silencing of the targeted gene compared to control mites fed non-specific lacZ dsRNA. In D. gallinae, dsRNA mediated gene knockdown is rapid, detectable 24 hours after oral delivery of dsRNA and persisted for at least 120 hours. Conclusions: This study has shown the presence of core RNAi machinery components in the D. gallinae genome. In addition, we have developed a robust RNAi methodology for targeting genes in D. gallinae, which will be of value for studying genes of unknown function and validating potential control targets in D. gallinae.

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