Category:Team Purple B 2018

Figure 3 shows the interaction between K74G BLIP (a beta-lactamase inhibitory protein mutant) with S. aureus PC1 wild-type β-lactamase and its A104E (beta-lactamase) mutant. K74G BLIP has greater inhibitory effect on the wild type beta-lactamase than the mutant beta-lactamase. Table 2 includes the inhibition constant of the purified K74G BLIP variant for PC1 β-lactamase, which shows about a 10-fold increase in comparison to that of wild type BLIP.

Table 2 compares NDM-1's antibiotic kinetics to other metallo beta-lactamases in K. pneumoniae and shows that the New Delhi metallo beta-lactamase has very little in common comparatively to the other MBLs. Specifically that NDM-1 shows higher affinity for cephalosporins than IMP-1 and VIM-2 given by its lower Km value.

• CORRECTION FOR ROUND 2 LAMBD:VINT*

Figure 3 shows that without the int gene, site-specific integration does not occur. Plasmids that did not contain the int gene did not perform recombination in the attB locus. There are 2 alternate start codons within the coding sequence for the int gene that are essential for integrase function. If there is a mutation in uoi, integrase still can function with the int gene. This proves that uoi is not required for integration in Mx8, but int is.

Only the C-terminal R153 residue is dispensable; there are lysis-defective nonsense mutations at positions 151 and 152 shown (Table 3) in the CTD region. A nonsense mutation (Rz C152X) shows the same effect as lysogen carrying an empty pRE plasmid vector (Vector), inhibiting cytolysis (Figure 3). The wild type pRz (WT), pRz with an artificial transmembrane domain (ART-TMD), and pRz 100–115 (Ser-Gly) show effective cytolysis in Figure 3.

repEA is an important gene in DNA synthesis and phage growth of phage T4. However, due to the amalgamation of several initiation sites in the T4 genome, mutations in repEA are not lethal. Nonsense mutations of repEA in conjunction with mot4 (to reduce initiation from different sources) mutations in phages showed smaller plaques compared to phages without both of these mutations (data not shown - from "Nonsense mutations in the repEA and repEB genes in combination with a motA mutation affect phage growth.")

The same repEA and mot4 mutation was shown to synthesize much less DNA compared to that of the phage with just the mot4 mutation (Figure 6), which was indicative of the importance of repEA versus other initiator proteins in DNA synthesis.