Disease relevance of ptsI

• Sugar transport by the bacterial phosphotransferase system. Molecular cloning and structural analysis of the Escherichia coli ptsH, ptsI, and crr genes [1].
• All of the 40 plaques examined contained phage able to transduce at least two of the genes known from bacteriophage P1 transduction experiments to be closely linked to ptsI [2].
• Single-crossover integration in the Lactobacillus sake chromosome and insertional inactivation of the ptsI and lacL genes [3].
• Unique dicistronic operon (ptsI-crr) in Mycoplasma capricolum encoding enzyme I and the glucose-specific enzyme IIA of the phosphoenolpyruvate:sugar phosphotransferase system: cloning, sequencing, promoter analysis, and protein characterization [4].
• Identification and characterization of two Alcaligenes eutrophus gene loci relevant to the poly(beta-hydroxybutyric acid)-leaky phenotype which exhibit homology to ptsH and ptsI of Escherichia coli [5].

High impact information on ptsI

• An Escherichia coli ptsI deletion grew on mannitol as the sole source of carbon after it was transformed with two compatible vectors; one vector encoded EI-N and the other encoded fusion Xa or fusion G [6].
• The crr promoters (P2) within ptsI may be negatively regulated by CRP.cAMP [7].
• Portions of the Salmonella typhimurium ptsI DNA sequence are known; the complete sequence is presented here and compared to Escherichia coli ptsI [8].
• The nucleotide sequences of ptsH, ptsI, and crr and the corresponding flanking regions have been determined [1].
• In addition, the ptsI gene contains two highly conserved direct repeats [1].

Chemical compound and disease context of ptsI

• The nucleotide sequence of an Escherichia coli DNA segment containing the ptsH gene and the first 162 nucleotides of the ptsI gene encoding, respectively, Hpr and enzyme I of the phosphoenolpyruvate-dependent glycose phosphotransferase system (PTS), was determined [9].
• The mutants showed the expected properties on PTS sugars, but in addition, ptsH and tight ptsI mutants were unable to utilize certain non-PTS sugars, including maltose, melibiose, glycerol, glycerol-P, mannose-6-P, and, in E. coli, lactose [10].
• Strain MM6-13 (ptsI suc lacI sup) of Escherichia coli contains a suppressor of the succinate-negative phenotype [11].
• The Bifidobacterium longum NCIMB 702259T ctr gene codes for a novel cholate transporter [12].

Biological context of ptsI

• Analysis of the nucleotide sequence substantiates the notion that the ptsH-ptsI-crr genes constitute a polycistronic operon [9].
• A cosmid containing the ptsH, ptsI and crr genes of Escherichia coli coding for three components of the phosphoenolpyruvate: sugar phosphotransferase system (PTS) has been isolated [13].
• The deletion covered a small fragment of the bacterial genome not extending in the ptsI and lig genes [14].
• Recombinant plasmids were constructed that carried various fragments of the DNA specifying the Escherichia coli genes ptsH and (part of) ptsI, the genes for the common components of the phosphoenolpyruvate: sugar phosphotransferase [15].
• The deduced amino acid sequences of ptsH and the N-terminal part of ptsI were compared to those of Streptococcus faecalis and Escherichia coli [16].

Associations of ptsI with chemical compounds

• The 1103 mutant with lack of enzyme 1 of the phosphoenolpyruvate-dependent phosphotransferase system (ptsI) behaves as well as P34 mutant after addition of glucose to casamino acids mineral medium [17].
• A ptsI mutant showed no chemotactic response to either glucose or PQQ alone but did show a chemotactic response to a mixture of glucose and PQQ [18].
• Similar results (no negative effect on pattern formation) were obtained with a ptsI mutant (defective in chemotaxis mediated by the phosphoenolpyruvate-dependent carbohydrate:phosphotransferase system [PTS]) and with addition of mannitol (a PTS ligand) to wild-type cells [19].
• Mutants that lack the genes ptsI and ptsH, which specify components of the PTS common to most PT-sugars, can mutate further to regain the ability to utilize fructose when this is present in relatively high concentration (i.e. greater than 2 mM) in the medium [20].
• These increased activities can explain the faster growth rate on ribose that was observed in ptsI mutants [21].

Other interactions of ptsI

• The gamma delta transposon studies also suggest that crr is transcribed from an independent promoter located within the ptsI gene [1].
• Mutations to loss of glucokinase, glk, are between the ptsI and dsd genes [22].
• Expression from the promoter region of the ptsH and ptsI genes has been studied in vivo by using gene fusions with lacZ [23].
• Two genes (ptsI and ptsA) that encode homologues of the energy coupling Enzyme I of the phosphoenolpyruvate-dependent sugar-transporting phosphotransferase system (PTS) have previously been identified on the Escherichia coli chromosome [24].

Analytical, diagnostic and therapeutic context of ptsI

• Northern blot analysis indicated that ptsI and crr constitute a dicistronic operon that includes an independent promoter for the crr gene [4].
• Reverse transcriptase PCR studies indicated that the four biosynthesis genes (synX to -D) and the capsule transport genes (ctr to -D) were separately transcribed as operons [25].

References