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Nuclease Tudor-SN Is Involved in Tick dsRNA-Mediated RNA Interference and Feeding but Not in Defense against Flaviviral or Anaplasma phagocytophilum Rickettsial Infection.

Authors :
Ayllón N
Naranjo V
Hajdušek O
Villar M
Galindo RC
Kocan KM
Alberdi P
Šíma R
Cabezas-Cruz A
Rückert C
Bell-Sakyi L
Kazimírová M
Havlíková S
Klempa B
Kopáček P
de la Fuente J
Source :
PloS one [PLoS One] 2015 Jul 17; Vol. 10 (7), pp. e0133038. Date of Electronic Publication: 2015 Jul 17 (Print Publication: 2015).
Publication Year :
2015

Abstract

Tudor staphylococcal nuclease (Tudor-SN) and Argonaute (Ago) are conserved components of the basic RNA interference (RNAi) machinery with a variety of functions including immune response and gene regulation. The RNAi machinery has been characterized in tick vectors of human and animal diseases but information is not available on the role of Tudor-SN in tick RNAi and other cellular processes. Our hypothesis is that tick Tudor-SN is part of the RNAi machinery and may be involved in innate immune response and other cellular processes. To address this hypothesis, Ixodes scapularis and I. ricinus ticks and/or cell lines were used to annotate and characterize the role of Tudor-SN in dsRNA-mediated RNAi, immune response to infection with the rickettsia Anaplasma phagocytophilum and the flaviviruses TBEV or LGTV and tick feeding. The results showed that Tudor-SN is conserved in ticks and involved in dsRNA-mediated RNAi and tick feeding but not in defense against infection with the examined viral and rickettsial pathogens. The effect of Tudor-SN gene knockdown on tick feeding could be due to down-regulation of genes that are required for protein processing and blood digestion through a mechanism that may involve selective degradation of dsRNAs enriched in G:U pairs that form as a result of adenosine-to-inosine RNA editing. These results demonstrated that Tudor-SN plays a role in tick RNAi pathway and feeding but no strong evidence for a role in innate immune responses to pathogen infection was found.

Details

Language :
English
ISSN :
1932-6203
Volume :
10
Issue :
7
Database :
MEDLINE
Journal :
PloS one
Publication Type :
Academic Journal
Accession number :
26186700
Full Text :
https://doi.org/10.1371/journal.pone.0133038