Category:Team Sexyback

Fig3B

Fig3B

Fig3A

Fig3A

Fig3A

Fig3A

Fig3, A&B

Fig3 A&B

Fig3 A&B

Fig3A

Fig3A

Figure 4A

Fig.4c

Fig2C

Fig2C

Fig1C

Fig1C

Fig2C

Fig. 1c

NTR:11338 modulation by virus of host cell type IV motility

Figure 3b and c shows the effects of truncated pilb genes. They are unable to restore the twitching ability to the pilB mutant,which implies the deleted regions are necessary for biogenesis of the pili

Fig6

Fig 4; panels C and D

Fig3, C

Fig6

Figure 5

Figure 5

Fig 1B shows sequence alignment, including highly conserved cysteine residue necessary for Ubiquitin thioester formation.

Fig 1B shows sequence alignment, including highly conserved cysteine residue necessary for Ubiquitin thioester formation.

Fig3 shows evidence for E3 Ubiquitin-protein ligase activty

Fig 1B shows sequence alignment, including highly conserved cysteine residue necessary for Ubiquitin thioester formation.

Fig 4b

Figure 3

Figure 4

Figure 6

Figure 4

Fig1 C

Fig1 C

Fig 4; panels C and D

Fig 6

Figure 3c

Figure 4b

Figure 4

Figure 3

Fig3 shows that MurJ activity is required for ColM dependent cleavage of lipidII in spheroplasts. When mutant MurJ(A29C) was inactivated with MTSES, flippase activity was reduced to a barely detectable level.

Fig4 panel B shows alignment of Cthe_2159 with D. dadantii Pectate lyase PelL. Despite very low identity for the rest of the protein, residues coordinating calcium in the primary calcium-binding site (Ca1) for Cthe_2159 and Pel9A and potential catalytic lysine side chains are nearly superimposable

Figure 2b-d

Figure 6, panel B. Mutant LolC(A40P)DE results in AcrA (an inner membrane protein) being localized to the outer membrane.