Category:Team Grapes of Staph

Fig. 1: the operator and the arrows indicate the direction of transcription from the two characterized of promoters.

Fig. 2 shows that the ainR mutant has decreased luminescence. This decreased luminescence can be mediated with the addition of C8-AHL. This shows that ainR in V. fischeri acts almost identically to luxN in V. harveyi.

Figure 2 shows the binding regulation of LuxR.

Figure 5 shows TEMs of the narrow columnar cells of the LuxA mutant infected squids vs the enlarged columnar cells of the wild type infected squids. The graph also depicts the decreased cytoplasmic volume between the two.

The table in Figure 5 shows the decreased levels of cytoplasm in the LuxR mutant vs the uninfected squids and wild type infected squids.

Figure 5 shows the different cytoplasmic volumes of the mutants and uninfected vs the wild type.

Table 1 shows that the LuxA gene is necessary for bioluminescence (not a regulator). Figure 2 also shows that biolumiscence is low in the LuxA mutants of the colonized juvenile squids in the experiment.

Fig 5, Table 2

Fig. 2 shows direct binding of LuxR protein to promoters of genes of Lux operon

Table 1 displays results of autoinducing molecules that can trigger the LuxR mutant into bioluminescing. Fig 2 signifies that when the luxR is not present the bioluminescence is significantly decreased in the colonized juvenile squids.

Table 1 shows that when autoinducers are introduced to the LuxI mutant then the bacteria will bioluminesce. Fig 2 signifies that when the luxI is not present the bioluminescence is significantly decreased in the colonized juvenile squid.

Table 3. Demonstrates how ainS mutants were unable to synthesize C8-HSL, preventing sufficient signalling to repress the LuxO repressor. This phenomenon resulted in a decrease in symbiotic luminescence.

A microarray study showed that the LuxR protein encoded by the luxR gene is a positive and negative regulator of different genes involved in bioluminescence.