Category:Team Simba's Pride

Figure 3 shows that XrvA contributes to the pathogenesis but is not completely dependent on it. Figure 5 also shows that XrvA has an influence on the expression levels of other known virulence genes.

Figure 5 shows that the Hpa2 protein is localized at the host cell membrane.

Figure 1 shows that HrpF1 contributes to pathogenesis of rice plants because it can compliment the double mutant of HrpF1 and Hpa2 (which is also shown to contribute to lesion formation).

Figure 5 shows that when HrpF1 is able to bind with Hpa2 in plant cells, it is localized in the plant cell membrane.

Figure 1 shows that Hpa2 contributes to pathogenesis of rice plants because it can compliment the double mutant of Hpa2 and HrpF (which is also shown to contribute to lesion formation).

Figure 2 shows that the ATP hydrolysis activity of the protein in vitro.

Figure 2 shows that when mutated, the host has significantly reduced symptom formation.

Figure 5 shows an immunoblot using antibodies against HrpE to show that the pilus is primarily composed of HrpE.

Figure 4 shows that a mutant hrpB cell has reduced entry into a host cell than compared to wild type.

Figure 2 shows systematic mutations in the protein sequence that affect virulence via interactions (or lack thereof) with HrcU, a known type III secretion protein

Figure 3 shows that HrcU does not prevent the expression of secreted proteins, but rather prevents the secretion of these proteins when mutated.

Figure 4 shows that when the gene is interrupted, the culture cannot grow on N-acetylglucosamine, showing an interruption in the metabolic pathway.

Figure 3 shows that when phaG is inturrupted, polyhydroxyalkanoate synthesis is inhibited.

Table 2 shows the beta-ketothiolase activity of the AM1 strain. It also shows the same activity of a phaB mutant and the no activity for a phaA mutant.

As shown in Figure 6, when grown in excess carbon the normal strain produced polyhydroxybutyrate granules but the mutant did not under the same conditions.