RESULTS
The first noticeable result was at first disappointing but turned around later in the trail. At first the rsaL mutation did not have any effect on the production of 30C12-HSL nor on lasl transcription, but it began to appear later in the logarithmic phase of propagation at which time the 30C12-HSL production along with Plasl activity reached homoeostasis in the wild strain while continuing to increase rsaL in the mutant strain of the pathogen. However the sturdy found that:
The increase in rsaL level coincides with the point at which the production of 30C12-HSL diverges in the parent and mutant strains. This is consistent with the conclusion that Rsal induction by 30C12-HSL results in sufficient Rsal to keep 30C12-HSL production at a steady level, balancing the positive feedback action on lasl expression (Rampioni, et. al. 1558)
From this the authors concluded that Rsal is the key molecule that effects the homeostasis of 30C12-HSL production. This could provide the first step in creating the quorum sensing trigger thereby effecting, halting and possibly even reversing the virulent reproduction of the pathogen's population.
The latter part of the previous conclusion is pointed out by the study as well. They believe that further findings suggest that RsaL is a negative autoregulator for the quorum sensing process. Their research has found that the binding of Rsal upon a unique site in the lasl-rsal inergenic region does trigger the divergent transcription on both of the genes sequencing. They refer to this area as Plasl or Prsal dependent on the consideration of the pasl or rsal being considered. There fore their final conclusion of these results is, "that the major funciont of Rsal in P. aeruginossp physiology is to govern the homeostasis of 30C12-HSL by controlling, in concert with Lasl, the expression of...
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