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What do we know about vector transmission of X. fastidiosa ?
Transmission of X. fastidiosa by sharpshooters is unique in terms of vector-pathogen relationships. Firstly, the interactions seem to be group-specific when compared to other systems, i.e. virtually all xylem sap-sucking insects can (and do) transmit different strains of X. fastidiosa. For example, members of the leafhopper family (Cicadellidae) in the sharpshooter subfamily (Cicadellinae), as well as spittlebugs (Cercopidae) and cicadas (Cicadidae) all transmit X. fastidiosa (see Almeida et al. 2005 for review). Different vector-strain-host plant combination may result in variable transmission efficiencies. The fact that sharpshooters transmit X. fastidiosa without specificity is well established (Almeida et al. 2005). Such lack of specificity suggests that
Vector-X. fastidiosa interactions are reasonably conserved among different taxa.
And that there is a general mechanism for pathogen attachment, multiplication and detachment.
The lack of transstadial transmission and latent period indicates that,
X. fastidiosa inoculum is limited to the foregut of vectors,
which is shed with each nymphal molt. Purcell et al. (1979) and Brlansky et al. (1983) showed the presence of X. fastidiosa in the cibarium and precibarium of vectors, corroborating the assumption that cells should be present in the foregut of infective individuals. Newman et al. (2003), using cells with a green fluorescent protein (GFP) marker, demonstrated the presence of cells in the precibarium of infective vectors. The direct association of the precibarium as the source of inoculum, however, has only been recently demonstrated. Newman et al. (2004) showed that non-transmissible X. fastidiosa mutants did not colonize the precibarium of vectors; and Almeida and Purcell (2006) showed that insects transmitting X. fastidiosa had the bacterium in their precibarium, whereas non-transmitting individuals did not. The later work strongly indicated that X. fastidiosa must attach to the precibarium of vectors to be inoculated into plants.
Why do we need to understand molecular aspects of X. fastidiosa transmission?
Current data suggest that X. fastidiosa is transmitted to plants from the precibarium of vectors where it attaches, multiplies, forms a ‘carpet’ of cells and eventually detaches to be injected into plants.
The details about the mechanics of an inoculation event (from the insect’s probing behavior perspective) are still to be determined.
In addition, there is no information on the interactions between X. fastidiosa and vectors.
To our knowledge, there is no datum on any molecular aspect of the vector-X. fastidiosa interface,
Except Newman et al. (2004) who demonstrated that a cell-cell signaling mutant is not transmissible (which showed that signaling controls transmission, but did not identify genes associated with attachment or retention per se). We intend to start to fill an essential gap in X. fastidiosa transmission and biology research with a study on the molecular determinants of the vector-pathogen interface. We also believe that new ideas and control strategies will emerge from this work because the molecular interactions in the vector-X. fastidiosa interface have never been studied.
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Glassy-winged Sharpshooter
Homalodisca coagulate
http://www.cnr.berkeley.edu/xylella/oss.htm
Formation of polar biofilm of Xylella fastidiosa in insect foreguts.
(Newman et al. 2004)
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