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. Author manuscript; available in PMC: 2013 Jan 6.
Published in final edited form as: Cell. 2012 Jul 6;150(1):222–232. doi: 10.1016/j.cell.2012.05.033

Figure 4. Cross-talk between PhoR(TV) and NtrX leads to a growth defect and fitness disadvantage in phosphate-limited media.

Figure 4

(A) Schematic of strains examined. In the wild type, PhoR-PhoB and NtrY-NtrX are insulated, whereas the PhoR(TV) mutant leads to cross-talk between PhoR and NtrX. (B) Doubling times of C. crescentus strains ΔphoR, ΔntrX, PhoR(TV), and PhoR(TV)/ΔntrX relative to wild type in M5G (phosphate-limited) and M2G (phosphate-replete) media. Error bars indicate standard errors, n=3. For growth curves in M8G medium (5 μM), see Figure S3A–B. (C) Wild type, ΔphoR, ΔntrX, PhoR(TV), and PhoR(TV)/ΔntrX were each competed against the wild type in M2GX and M5GX. The percentage of mutant cells in the population was measured periodically for 104 hours. Curves represent the average of two independent competitions with swapped fluorophores. Also see Figure S3C–D. (D) Expression data for known members of the pho regulon in PhoR(TV) and ΔphoR in M2G (phosphate-replete) media. Data are expressed as log2 values of the ratio between a given mutant and wild-type C. crescentus, and are color-coded according to the legend. (E) Time courses of phosphotransfer from kinases PhoR(TV) and NtrY to the regulators NtrXΔC and an NtrXΔC harboring β-like specificity substitutions. Only the response regulator band is shown.