Investigation on methods related to quorum sensing between bacterial cells to direct and synchronize communal behavior and the manifestation of potent features has led them to come across a way to block the communication between bacterial cells.
A research team formed by the molecular biology department at the Princeton University and the Howard Hughes Medical Institute have published their findings in a paper that is titled, “A Strategy for Antagonizing Quorum Sensing,” in the Molecular Cell.
The communication mechanism of quorum-sensing by bacterial cells is done through autoinducer molecules. Of the bacterial cells, the Gram negative cells use acyl-homoserine lactone molecules (AHLs) as autoinducers and the detection is done in different ways by different cells. One of the mechanisms is by using cytoplasmic LuxR-type transcription factor proteins as receptors. Of these chlorolactone LuxR acted against the human pathogen Chromobacterium violaceum from destroying Caenorhabditis elegans. The researchers observed that in the Chromobacterium violaceum bacteria, the autoinducers get attached to the LuxR-type transcription factor protein CviR. The LuxR-type proteins are classified as homodimers having two monomers, each having a ligand-binding domain (LBD) and a DNA binding domain (DBD).
The constitutional operation analysis was done on both natural and artificial ligands to CviR. The study on the CviR chlorolactone antagonist revealed that binding factor CviR was opposed by the molecules that unite instead of the acytylated homoserine lactone autoinducer. This opposition was present until the antagonist binding brought about a closed shape that was not capable of binding to the DNA. Therefore, the structure of the antagonist-bound CviR was arrayed in such a manner that the DBD of each monomer, was below the LBD of the opposite monomer in a crossed-domain fashion. This formation blocked the opposing ligand-binding areas. The research team concentrated on this binding concept and came up with two strategies for blocking the quorum sensing in bacteria. One was to identify the ligands that take the place of the autoinducer and play the role of inactivating the LBD-DBD interaction. Another concept was to find out, which molecules bind to the pre-formed LuxR-autoinducer in order to form closed shapes. The second case however does not have practical examples.
Source: http://www.princeton.edu/main/