Category:Team The Schmosbies

VP35 binds to a polyCG dsRNA linked to agarose beads, while it does not interact with the agarose beads without RNA (Fig. 4A, lanes 1 and 2).

Figure 2. (A-E)

(A) Wild-type F. johnsoniae UW101 without gldJ. (B) Wild-type cells gldJ. (C) gldJ mutant UW102-48 without gldJ. (D) UW102-48 complemented with pMM313 that carries gldJ. (E) Wild-type cells, which carries a truncated version of gldJ.

Figure 5:

Portion H-/+ Mutations in GldH show absence of chitinase activity, compared to when glDH mutants are co-expressed with plasmids containing GldH.

Figure 2.

Shows that wild type strain has gliding motility (A). Mutants do not (B). Mutants treated with plasmid containg GldH recover motility(C). Plasmids without GldH do not recover motility (D).

Figure 5. Portion B.

Video showing tracts of cell movement compared to the wild phenotype, show decreased motility in cells with mutations in SprC.

Figure 5: Tracks illustrating the movements of the cells shown in panels A to I over a 60-s period were obtained by superimposing individual digital video frames over Palmer cell slides showed decreased motility in SprD as compared to the wild type, which was shown in portion F of figure 5.

Figure 5. Panel B: MprD null mutants are unable to grow in the sodium rich environments compared to both wild type cells and cells with MprD placed back into the cells via a plasmid.

Figure 5.

Panel A: MprA null mutants are unable to grow in the sodium rich environments compared to both wild type and cells with MprA placed back into the cells via a plasmid.

Figure 3.

Two strains of the Fungus Rhizopus mycelium were tested in a control and experimental group. The experimental groups with CSNV26 expressed had deformed the chitosan cell walls of the fungi.

Figure 5 shows an immunoprecipitation, demonstrating that without gBP21, the RNA no longer has separation from editing.

Figure 4 shows U-deletion cleavage activity of rTbMP90 (also known as KREPB1). Deletion of this is used, mutating the trypanosomes and changing the phenotype as a result.

Using figures 2 and 3 to determine the function for PTR1. Figure 2 shows the production of tetracycline with and without PTR1 in the cells and their resulting virulence in Figure 4. Figure 3 shows the enzyme activity of PTR1.

Figures 5 A and B. FlgM shows higher miller unit activity compared to control

Fig 1.C. Mutations were engineered into fLHO and expression of mutant reduced swarm motility.

Fig. 1C shows that a mutation in fliK abolished the swarming motility observed in WT cells.