Presentation is loading. Please wait.

Presentation is loading. Please wait.

Fig. 3. Phenotypic characterization of FM2.5.

Published byRodney McCoy Modified over 5 years ago

Similar presentations

Presentation on theme: "Fig. 3. Phenotypic characterization of FM2.5."— Presentation transcript:

1 Fig. 3. Phenotypic characterization of FM2.5.
Phenotypic characterization of FM2.5. (A and B) Cultures of R20291, FM2.5, and FM2.5RW were challenged with lysozyme (500 μg/ml) (A) or LL-37 (5 μg/ml) (B) in exponential phase after 2.5 hours (indicated with arrows). Untreated control cultures were grown in parallel. Experiments were carried out in triplicate on biological duplicates. Means and SDs are shown. (C) Sporulation of R20291, FM2.5, and FM2.5RW after 5 days. Spore CFUs were determined after a standard 65°C heat treatment for 30 min or a harsher 75°C heat treatment for 30 min. Heat-resistant spore CFUs are expressed as a percentage of total viable CFUs (spores and vegetative cells). Experiments were carried out in triplicate on biological duplicates. Means and SDs are shown. *P < 0.01, determined using two-tailed t tests with Welch’s correction. (D) Germination of R20291, FM2.5, and FM2.5RW spores. Synchronous germination of purified spores was induced with the bile salt taurocholate. Germination initiation was monitored by measuring the resulting decrease in OD600nm. Joseph A. Kirk et al., Sci Transl Med 2017;9:eaah6813 Published by AAAS

Download ppt "Fig. 3. Phenotypic characterization of FM2.5."

Similar presentations

Fig. 6. Sh-lantibiotics are commonly found on healthy human skin and synergize with a host AMP. Sh-lantibiotics are commonly found on healthy human skin.

Fig. 6. Sh-lantibiotics are commonly found on healthy human skin and synergize with a host AMP. Sh-lantibiotics are commonly found on healthy human skin.
Fig. 2. Effects of AZD4785 on proliferation and MAPK pathway signaling in KRAS mutant and wild-type cancer cells in vitro. Effects of AZD4785 on proliferation.

Fig. 2. Effects of AZD4785 on proliferation and MAPK pathway signaling in KRAS mutant and wild-type cancer cells in vitro. Effects of AZD4785 on proliferation.
Fig. 5. S. hominis A9 isolated from normal human skin produces unique lantibiotics. S. hominis A9 isolated from normal human skin produces unique lantibiotics.

Fig. 5. S. hominis A9 isolated from normal human skin produces unique lantibiotics. S. hominis A9 isolated from normal human skin produces unique lantibiotics.
Fig. 1. IL-6 is associated with resistance to EGFR TKIs and is induced by stress hormones. IL-6 is associated with resistance to EGFR TKIs and is induced.

Fig. 1. IL-6 is associated with resistance to EGFR TKIs and is induced by stress hormones. IL-6 is associated with resistance to EGFR TKIs and is induced.
Fig. 6. AZD6738 induces DNA damage and apoptosis and exhibits antitumor efficacy in xenograft models of high-risk medulloblastoma and neuroblastoma. AZD6738.

Fig. 6. AZD6738 induces DNA damage and apoptosis and exhibits antitumor efficacy in xenograft models of high-risk medulloblastoma and neuroblastoma. AZD6738.
Differentiation of AZD4785 from MAPK pathway inhibitors in vitro

Differentiation of AZD4785 from MAPK pathway inhibitors in vitro
Fig. 1. The cell-intrinsic fibroblast circadian proteome contains numerous cytoskeletal regulators. The cell-intrinsic fibroblast circadian proteome contains.

Fig. 1. The cell-intrinsic fibroblast circadian proteome contains numerous cytoskeletal regulators. The cell-intrinsic fibroblast circadian proteome contains.
Fig. 2. Pharmacologic inhibition of ALK impairs STING activation.

Fig. 2. Pharmacologic inhibition of ALK impairs STING activation.
Fig. 2. Mechanism of PD-L1 down-regulation in NOD HSPCs.

Fig. 2. Mechanism of PD-L1 down-regulation in NOD HSPCs.
Fig. 3. Antimicrobial activity is detected in diverse strains of CoNS and not predictable at the species level. Antimicrobial activity is detected in diverse.

Fig. 3. Antimicrobial activity is detected in diverse strains of CoNS and not predictable at the species level. Antimicrobial activity is detected in diverse.
Fig. 5 Maraba induces antitumor T cell immunity.

Fig. 5 Maraba induces antitumor T cell immunity.
Fig. 4. Specific antibiotics reduce fecal biomass in mice and humans.

Fig. 4. Specific antibiotics reduce fecal biomass in mice and humans.
Fig. 2. dAST using dPCR is robust to the presence of high concentrations of commensal bacteria due to the specificity of NA amplification. dAST using dPCR.

Fig. 2. dAST using dPCR is robust to the presence of high concentrations of commensal bacteria due to the specificity of NA amplification. dAST using dPCR.
Fig. 1 Increasing UCB cell dose impairs short-term progenitor cell engraftment. Increasing UCB cell dose impairs short-term progenitor cell engraftment.

Fig. 1 Increasing UCB cell dose impairs short-term progenitor cell engraftment. Increasing UCB cell dose impairs short-term progenitor cell engraftment.
Fig. 2 TLR8 is aberrantly expressed on pDCs from SSc patients.

Fig. 2 TLR8 is aberrantly expressed on pDCs from SSc patients.
Fig. 2 Maraba treatment results in complete responses in the window of opportunity setting. Maraba treatment results in complete responses in the window.

Fig. 2 Maraba treatment results in complete responses in the window of opportunity setting. Maraba treatment results in complete responses in the window.
Fig. 3. A circadian rhythm in fibroblast wound-healing response.

Fig. 3. A circadian rhythm in fibroblast wound-healing response.
Fig. 8. mRIPO elicits neutrophil influx followed by DC and T cell infiltration into tumors. mRIPO elicits neutrophil influx followed by DC and T cell infiltration.

Fig. 8. mRIPO elicits neutrophil influx followed by DC and T cell infiltration into tumors. mRIPO elicits neutrophil influx followed by DC and T cell infiltration.
Fig. 1 DMF promotes viral infection.

Fig. 1 DMF promotes viral infection.
Fig. 3 TLR8 signaling induces CXCL4 and IFN-α secretion by SSc PDCs.

Fig. 3 TLR8 signaling induces CXCL4 and IFN-α secretion by SSc PDCs.

Similar presentations

Ads by Google