I am attempting to write a grant proposal for a class that aims to look at the protein-proteins interactions of the T4SS effector BspC and Golgi proteins such as GM130. It has been shown that out of the 5 well characterized Brucella effectors, BspC is the only effector that localizes to the Golgi, while all other effectors localize to the ER. This makes sense since the BCV associates almost exclusively with the ER during replication, and the membrane contains many ER markers in order to accomplish this. BUT what I don't understand and would like to look into is why a T4SS effector would localize to the Golgi, where the BCV is not associated. I understand that Rab2, utilized by BCV, is derived from the Golgi, but that is the extent of the interaction that I am aware occurs between Brucella and the Golgi. Is it possible that the T4SS effector localizes to the Golgi in order to recruit the premature BCV to the Golgi so that it can obtain Golgi markers like Arf and Rab in order to facilitate hacking into the retrograde transport system from the Golgi to the ER, such that the the premature BCV then comes into contact with the ER, gains ER markers, and then matures into a replicating BCV? Does anybody who has experience with Brucella abortus, Chlamydia, or Legionella pneumophila pathogenesis (which use similar pathogenic pathways to target the secretory pathway) know why this phenomena might be happening? In the context of retrograde transport or autophagy perhaps. I would greatly appreciate any help that I can get.