@article{mbs:/content/journal/micro/10.1099/00221287-145-11-3195, author = "Martin-Verstraete, Isabelle and Galinier, Anne and Darbon, Emmanuelle and Quentin, Yves and Kilhoffer, Marie-Claude and Charrier, Véronique and Haiech, Jacques and Rapoport, Georges and Deutscher, Josef", title = "The Q15H mutation enables Crh, a Bacillus subtilis HPr-like protein, to carry out some regulatory HPr functions, but does not make it an effective phosphocarrier for sugar transport", journal= "Microbiology", year = "1999", volume = "145", number = "11", pages = "3195-3204", doi = "https://doi.org/10.1099/00221287-145-11-3195", url = "https://www.microbiologyresearch.org/content/journal/micro/10.1099/00221287-145-11-3195", publisher = "Microbiology Society", issn = "1465-2080", type = "Journal Article", keywords = "HPr, histidine-containing protein", keywords = "PEP, phosphoenolpyruvate", keywords = "FPr, fructose-specific HPr", keywords = "NPr, nitrogen-related HPr", keywords = "PTS, PEP:sugar phosphotransferase system", keywords = "PEP:sugar phosphotransferase system", keywords = "catabolite repression", keywords = "Crh", keywords = "HPr", abstract = "Crh of Bacillus subtilis exhibits 45% sequence identity when compared to histidine-containing protein (HPr), a phosphocarrier protein of the phosphoenolpyruvate (PEP):sugar phosphotransferase system (PTS). Crh can be phosphorylated by ATP at the regulatory Ser-46 and similar to P-Ser-HPr, P-Ser-Crh plays a role in carbon-catabolite repression. The sequence around the phosphorylatable Ser-46 in Crh exhibits strong similarity to the corresponding sequence of HPr of Gram-positive and a few Gram-negative bacteria. In contrast, the catalytic His-15, the site of PEP-dependent phosphorylation in HPr, is replaced with a glutamine in Crh. When Gln-15 was exchanged for a histidyl residue, in vitro PEP-dependent enzyme I-catalysed phosphorylation of the mutant Crh was observed. However, expression of the crhQ15H mutant allele did not restore growth of a ptsH deletion strain on the PTS sugars glucose, fructose or mannitol or on the non-PTS sugar glycerol. In contrast, Q15H mutant Crh could phosphorylate the transcriptional activator LevR as well as LevD, the enzyme IIA of the fructose-specific lev-PTS, which together with enzyme I, HPr and LevE forms the phosphorylation cascade regulating induction of the lev operon via LevR. As a consequence, the constitutive expression from the lev promoter observed in a ΔptsH strain became inducible with fructose when the crhQ15H allele was expressed in this strain.", }