29 research outputs found

    Additional file 1: Table S1. of Comparative genomics analysis of triatomines reveals common first line and inducible immunity-related genes and the absence of Imd canonical components among hemimetabolous arthropods

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    Immunity-genes reference dataset. Dataset of immunity-genes sequences retrieved from GenBank, VectorBase, UniProt, FlyBase and Ensembl databases and published information used to query for immune-related homologs in TTTs transcriptomes and RPRO, CLEC and ACPI predicted-peptide sets. Table S2. Immune-related homologs involved in immune recognition and activation (PGRPs; GNBPs; Lectins; TEPs; Scavenger receptors; Clip-domain serine-proteases) and their respective transcriptome/genome sequence-IDs in the six hemipteran species. Table S3. Immune-related homologs involved in immune signaling (Toll, Jak-STAT and Imd pathways) and their respective transcriptome/genome sequence-IDs in the six hemipteran species. Table S4. Immune-related homologs involved in immune effectors (antimicrobial peptides; PPOs; nitric oxide synthase; NADPH enzymes) and their respective transcriptome/genome sequence-IDs in the six hemipteran species. Table S5. Immune-related homologs involved in immune regulation (immune negative regulators) and their respective transcriptome/genome sequence-IDs in the six hemipteran species. Table S6. Immune-related homologs involved in antioxidant mechanisms (Catalases; Peroxidases) and their respective transcriptome/genome sequence-IDs in the six hemipteran species. Table S7. Immune-related homologs involved in RNA interference (RNAi machinery components) and their respective transcriptome/genome sequence-IDs in the six hemipteran species. Table S8. Immune-related homologs involved in coagulation (Fondue and Hemolectin proteins) and their respective transcriptome/genome sequence-IDs in the six hemipteran species. (XLSX 53 kb

    Data_Sheet_1_De Novo DNA Synthesis in Aedes aegypti Midgut Cells as a Complementary Strategy to Limit Dengue Viral Replication.xlsx

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    <p>Aedes aegypti is the main vector of Dengue Virus, carrying the virus during the whole mosquito life post-infection. Few mosquito fitness costs have been associated to the virus infection, thereby allowing for a swift dissemination. In order to diminish the mosquito population, public health agency use persistent chemicals with environmental impact for disease control. Most countries barely use biological controls, if at all. With the purpose of developing novel Dengue control strategies, a detailed understanding of the unexplored virus-vector interactions is urgently needed. Damage induced (through tissue injury or bacterial invasion) DNA duplication (endoreplication) has been described in insects during epithelial cells renewal. Here, we delved into the mosquito midgut tissue ability to synthesize DNA de novo; postulating that Dengue virus infection could trigger a protective endoreplication mechanism in some mosquito cells. We hypothesized that the Aedes aegypti orthologue of the Drosophila melanogaster hindsight gene (not previously annotated in Aedes aegypti transcriptome/genome) is part of the Delta-Notch pathway. The activation of this transcriptional cascade leads to genomic DNA endoreplication. The amplification of the genomic copies of specific genes ultimately limits the viral spreading during infection. Conversely, inhibiting DNA synthesis capacity, hence endoreplication, leads to a higher viral replication.</p

    Oligonucleotide sequences used in this study.

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    *<p>Underlined nucleotides indicate the stop codon for mutagenesis in positions 823–825.</p><p>AdaptAFlx refers to the 454 adaptor A sequence. AdaptAFlx refers to the 454 adaptor B sequence. 454 key indicates 454 library key sequence (TCAG). Nucleotides in bold italics indicate barcodes. Regular font indicates NA gene specific sequence (699–716; 983–1000).</p

    Sequence coverage plots of the sequenced NA amplicon according to barcode (A) and according to picotiterplate region (B).

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    <p>Positions of the NA gene are shown in X axis, whereas the number of reads is shown in Y axis. Less variability in read number was obtained according to MID than according to sequencing region, suggesting that the source of variability is during the emPCR amplification.</p
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