In Objectives 1 and 2, we proposed targeting specific regulators of key phage encoded virulence genes (such as the Las LexA-like repressor, LC1, a second downstream repressor, LC2, controlled in part by LC1), and a key exogenous regulator of the (lethal) phage lytic cycle encoded by Wolbachia, an important psyllid endosymbiont that is always found when Las is present. These results have so far resulted in three full length manuscripts and 14 abstracts. LC1, LC2 and the Wolbachia repressor have all been confirmed to be transcriptional repressors. All three are therefore prime targets for chemical interference. Purchase orders to have these three repressors commercially produced by synthesized were placed several months ago and all three have finally now been delivered. Both the LC1 and the Wolbachia repressor were charactereized by the commercial vendors as “difficult” to synthesize. Attempts in our lab to synthesize LC1 and the Wolbachia repressor indicated that both cause E. coli host cells to become quite “sick”, with very slow growth, likely because of the repressors’ effects on E. coli host gene regulation. These proteins were synthesized in vitro for evaluation purposes, but this is expensive for the scale needed for chemical screening purposes and slow delivery of the repressor proteins was not anticipated. Two versions of the Wolbachia repressor were delivered. One version, with a histidine (HIS) tag, failed to repress the Las target promoter, probably due to the presence of the tag. The native version, without the tag, worked as expected from the in vitro results. Chemical screening assays are now underway with all three. The Wolbachia protein has been shipped to both the De La Fuente lab in Auburn, and Duan lab at USDA-Ft. Pierce, our collaborators on a separate culturing project.