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Title: Silencing of a putative immunophilin gene in the cattle tick Rhipicephalus (Boophilus) microplus increases the infection rate of Babesia bovis in larval progeny

Author
item BASTOS, REGINALDO - Washington State University
item UETI, MASSARO - Washington State University
item Guerrero, Felicito
item Knowles Jr, Donald
item Scoles, Glen

Submitted to: Parasites & Vectors
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/16/2009
Publication Date: 11/20/2009
Citation: Bastos, R.G., Ueti, M.W., Guerrero, F., Knowles Jr, D.P., Scoles, G.A. 2009. Silencing of a putative immunophilin gene in the cattle tick Rhipicephalus (Boophilus) microplus increases the infection rate of Babesia bovis in larval progeny. Parasites & Vectors. 2:article 57.

Interpretive Summary: The cattle tick Rhipicephalus (Boophilus) microplus is involved in the transmission of the protozoan Babesia bovis, the causative agent of bovine babesiosis, or cattle fever. Interactions between ticks and microorganisms are poorly understood, particularly the investigation of tick genes that affect tick fitness and microbial infection. In this study, RNA interference was used to silence R. microplus genes that had been previously shown to be up-regulated in response to B. bovis infection. Immunophilins are a family of very conserved proteins with various functions in cells, including transport, binding, and response to metabolic stress. The silencing of a gene encoding an immunophilin in female ticks fed on a B. bovis infected calf decreased the hatching rate and survival of larval progeny. Interestingly, immunophilin was upregulated significantly in ovaries of R. microplus in response to B. bovis infection and this silencing experiment significantly increased the infection rate of B. bovis in larval progeny. The results also showed that the silencing of two other genes, including a Kunitz-type serine protease inhibitor (Spi) gene and a lipocalin (Lpc) gene also decreased the fitness of R. microplus female ticks, but, unlike the immunophilin result, had no significant effect on the infection rate of B. bovis in larval progeny. The silencing of the immunophilin, Spi or Lpc genes decreased the fitness of R. microplus females fed on a calf during acute B. bovis infection. The immunophilin gene data suggest that this gene is involved in the defense system of R. microplus against B. bovis and may play a role in controlling the protozoan infection in tick ovaries and larvae progeny.

Technical Abstract: The cattle tick Rhipicephalus (Boophilus) microplus is involved in the transmission of the protozoan Babesia bovis, the etiological agent of bovine babesiosis. Interactions between ticks and protozoa are poorly understood and the investigation of tick genes that affect tick fitness and protozoan infection can set the stage for dissecting the molecular interactions between the two species. In this study, RNA interference was used to silence R. microplus genes that had been previously shown to be up-regulated in response to B. bovis infection. The silencing of a putative immunophilin gene (Imnp) in female ticks fed on a calf acutely infected with B. bovis decreased the hatching rate and survival of larval progeny. Interestingly, Imnp was upregulated significantly in ovaries of R. microplus in response to B. bovis infection and its silencing in female ticks significantly increased the infection rate of the protozoan in larval progeny. The results also showed that the silencing of a putative Kunitz-type serine protease inhibitor (Spi) gene and a putative lipocalin (Lpc) gene decreased the fitness of R. microplus females, but had no significant effect on the infection rate of B. bovis in larval progeny. The silencing of the Imnp, Spi or Lpc genes decreased the fitness of R. microplus females fed on a calf during acute B. bovis infection. The Imnp gene data suggest that this putative immunophilin gene is involved in the defense system of R. microplus against B. bovis and may play a role in controlling the protozoan infection in tick ovaries and larvae progeny.