Data are fully supported by previous studies by Kao KC, 2004 aimed at the determination of Transcription Factor Activities (TFAs) and gene expression profiles, particularly after a transition from glucose to acetate. Thus the level of CRP was shown to peak within the first hour of transition and gradually reduce after an hour. The gene expression profile of pckA indicated a similar time scale, pckA being down-regulated within the first hour (after 5 minutes of the transition) and up-regulated gradually after an hour. This 'Cyclic AMP Responsive Switching' is particularly interesting as it bears consequences for analyzing the drastic downshift from glucose to acetate.
BMC Syst Biol. 2014Sorbitol (also known as glucitol) is classified by the authors as a non-PTS sugar. However, it is a PTS sugar for Escherichia coli (Lengeler J, 1975). Its transport causes PTS-linked regulations. This error was carried on by Koirala S, 2016. In relation to sorbitol being a PTS sugar, Shiga toxin-producing E. coli O55:H7 does not ferment sorbitol due to a nonsense mutation in srlA encoding Enzyme IICSrl (Schutz K, 2017).
Microbiol Mol Biol Rev. 2014This review was released for the 50th anniversary of the discovery by Kundig, Ghosh and Roseman of a novel 'phospho-transferase system', presently defined as the phosphotransferase system or PTS. In a 1964 landmark paper, the pioneers remarkably characterized the protein-bound phosphohistidine (P-HPr), and demonstrated phosphoenolpyruvate (PEP) could act as the initial phosphoryl donor for their purified PTS proteins, which included the Enzymes I and II. They further indicated PTS substrates were D-sugars, the product formed from glucose was glucose 6-phophate, and more than one Enzyme II could be synthesized by the cell.
In relation to the regulatory functions of the PTS, regulation of adenylate cyclase by phosphorylated Enzyme IIAGlc was poorly addressed by the authors of the review, they referred to an inadequate paper by Krin E, 2002, which addresses the role of the histone-like protein H-NS on the cAMP levels. That paper main conclusion was adenylate cyclase is not fully activated in a crp hns double mutant strain (lacking both CRP and H-NS) due to a reduced expression of crr which encodes EnzymeIIAGlc, a conclusion to be taken with caution considering the more than two-fold decrease in expression of the adenylate cyclase gene in the double mutant.
In relation to diauxie, the authors stated, "cAMP formation seems to affect the lag phase" and "addition of extracellular cAMP either shortens or entirely eliminates the lag phase". In fact, addition of cAMP does not always shorten or eliminate the lag phase, for example the glucose-galactose diauxie. The authors also stated, "addition of extracellular cAMP cannot prevent CCR [Carbon Catabolite Repression]" however the reference to support the authors' statement is not appropriate, the strain used by Kimata K, 1997 is impaired in β-galactosidase synthesis (Crasnier-Mednansky M, 2008), and the contention that inducer exclusion is the major CCR mechanism in E. coli was based on a flawed paper by Inada T, 1996 (Diauxie correspondence).