Category:Team Francis Crick

Figure 2b and C FtsZ labeled with GDP for flourences, shows formation of ring during intermediate and late stages of division, indication of involvement in cytokinesis.

Figure 2b and C FtsZ labeled with GDP for flourences, shows formation of ring during intermediate and late stages of division.

Furthermore, the experiment using the OmpA-deficient mutant

HN742 (Fig. 6) showed conclusively that the channel formation was caused by OmpA, denaturation of OmpA essentially abolished the solute diffusion process and that nonporin proteins such as bovine serum albumin could not facilitate the solute diffusion across the membrane.

SulA inhibits the assembly of FtsZ, preventing the cells from performing cytokenesis. Figure 8E showing the increase in SulA,causes a decrease in FtsZ formation. Figure 6 EM images of PaFtsZ and the inhibition of assemble by SulA. Figure 1 (a,b) EM images of ECFtsZ without SulA and with the indicated addition of SulA

Deletion leads to impaired septa formation Fig 2, as well as slowed growth.

Shown that B. subtilis FtsA is capable of binding and hydrolysing ATP (Fig. 7), To test whether FtsA has ATPase activity, a measurement of the hydrolysis of ATP by monitoring the release of 32Pi from [γ-32P]-ATP. The activity was readily detected, and analysis of the reaction revealed Michaelis–Menten kinetics (Fig. 7B) with a Km of 0.7 mM and a Vmax of 0.125 mol of ATP hydrolysed per second per mol of FtsA dimer.

Culturing of yceP mutants and wild-type strain in LB did not lead to a variation in observed biofilm formation while twofold (P = 0.052) and threefold (P = 0.001) increases in biofilm occurred in LB glu upon deletion of yceP (Figure 1A). Lastly when biofilm formation was observed in a continuous flow system in M9C glu medium, the yceP deletion caused the cells to form a more random, scattered, and globular biofilm with far less surface coverage (Figure 2B).

Figure 6 and figure 7 display unbalanced cell growth and division in the absence of StkP. Wild-type cells were able to develop one cell-division ring in the center while cells with mutated strains became over-elongated and formed multiple rings, leading to division into more than two daughter cells.

Figure 8 shows that SasG-expressing SH1000 cells form a biofilm measured with crystal violet staining and read at A570. SH1000 variants carrying pALC2073 expressing SasG with eight, six and five B repeats resulted in the formation of a biofilm. Strains expressing four, two or one B repeats did not form biofilms (Fig. 8c)

Figure 1 displays how Pard6b knockdown suppresses formation of the blastocyte cavity, although it does not affect early blastomere cleavages in embryo (Table 1).