Therefore it is imaginable that internalized c-synuclein abs bind their antigen and alter its function. The modulated function of c-synuclein could lead to a changed binding of transcription factors and therefore to a changed expression of mitochondrial apoptosis proteins. Future experiments are needed to provide more information about the exact mechanisms. Arthropod vectors transmit a diversity of animal and human pathogens, ranging from RNA viruses to LY294002 protozoal parasites. Chemotherapeutic control of pathogens has classically focused either on insecticides that kill the vector itself or antimicrobials for infected patients. The limitation of the former is that it targets both infected and uninfected vectors and thus broadly selects for resistant populations while the latter requires prompt and accurate diagnosis. An alternative strategy is to target vector molecules that permit the pathogen to establish itself, replicate, and/or develop within the vector, thus specifically targeting only the small proportion of infected vectors. Vector competence, the ability to acquire and transmit pathogens, is a multifactorial process and involves multiple genes and gene networks in multiple organs. The vector midgut and salivary glands are attractive targets as these organs represent, respectively, sites of initial colonization and secretion into the saliva for transmission. Using the rickettsial pathogen Anaplasma marginale and its tropical tick vector, Rhipicephalus microplus, as a model, we previously identified a set of tick midgut and salivary gland genes that are regulated in response to pathogen infection. We supplemented this set with R. microplus genes for which the expressed protein has been shown to vary in response to babesial infection. Six candidate genes were selected based on bioinformatics analysis and an initial screen using post-transcriptional gene silencing by small interfering RNA. Silencing of these six genes was then used to test two related hypotheses in the A. marginale/R. microplus model. The first was that silencing of the selected R. microplus genes affects the A. marginale infection rate in the tick midguts or salivary glands. The second hypothesis was that silencing of the selected R. microplus genes affects the level of A. marginale within infected ticks. Herein, we present the results of these experiments and discuss the findings in the context of the interface between tick biology and pathogen transmission. Glutamine synthetase plays an essential role in the metabolism of nitrogen by catalyzing the condensation of glutamate and ammonia to form glutamine, protecting the cell against excitotoxicity, or other adaptations that alleviate high levels of glutamate and ammonia. In murine models of malaria and in Schistosoma mansoni infection of its molluscan host Biomphalaria glabrata, infection was associated with increased glutamine synthetase expression, suggested to be a protective mechanism against infection-induced increases in glutamate levels. The increased A. marginale infection rates upon TC17129 silencing in R. microplus ticks would be consistent with this role.