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Literature summary for 2.7.8.43 extracted from
- Activation of PmrA inhibits LpxT-dependent phosphorylation of lipid A promoting resistance to antimicrobial peptides (2010), Mol. Microbiol., 76, 1444-1460.
Activating Compound
| Activating Compound | Comment | Organism | Structure |
|---|---|---|---|
| PmrA | te enzyme EptA is activated in a PmrA-dependent manner, overview | Escherichia coli |
Inhibitors
| Inhibitors | Comment | Organism | Structure |
|---|---|---|---|
| LpxT | role for LpxT in the reduction of enzyme EptA activity, the transcriptional regulation of lpxT gene is PmrA-independent. PmrA-dependent inhibition of LpxT is required for phosphoethanolamine decoration of lipid A | Escherichia coli | |
| LpxT | role for LpxT in the reduction of enzyme EptA activity. Loss of Salmonella lpxT greatly increases modification of lipid A through enzyme EptA. LpxT catalyses the phosphorylation of lipid A at the 1-position | Salmonella enterica |
Localization
| Localization | Comment | Organism | GeneOntology No. | Textmining |
|---|---|---|---|---|
| periplasm | - |
Salmonella enterica | - |
- |
| periplasm | - |
Escherichia coli | - |
- |
Metals/Ions
| Metals/Ions | Comment | Organism | Structure |
|---|---|---|---|
| Fe3+ | required, the peptA (eptA promoter) is induced sevenfold in the presence of Fe3+ | Escherichia coli |  |
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Escherichia coli | P30845 | W3110, gene eptA or pmrC | - |
| Salmonella enterica | P36555 | serovar typhimurium, gene eptA or pmrC | - |
| Salmonella enterica LT2 | P36555 | serovar typhimurium, gene eptA or pmrC | - |
Substrates and Products (Substrate)
| Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
|---|---|---|---|---|---|---|
| additional information | enzyme EptA catalyses the periplasmic addition of the positively charged substituent phosphoethanolamine to lipid A controlled by the PmrA transcriptional regulator and conferring resistance to cationic antimicrobial peptides, including polymyxin | Salmonella enterica | ? | - |
? | |
| additional information | enzyme EptA or PmrC catalyses the periplasmic addition of the positively charged substituent phosphoethanolamine to lipid A controlled by the PmrA transcriptional regulator and conferring resistance to cationic antimicrobial peptides, including polymyxin | Escherichia coli | ? | - |
? | |
| additional information | enzyme EptA catalyses the periplasmic addition of the positively charged substituent phosphoethanolamine to lipid A controlled by the PmrA transcriptional regulator and conferring resistance to cationic antimicrobial peptides, including polymyxin | Salmonella enterica LT2 | ? | - |
? | |
Synonyms
| Synonyms | Comment | Organism |
|---|---|---|
| EptA | - |
Salmonella enterica |
| EptA | - |
Escherichia coli |
| PmrC | - |
Salmonella enterica |
| PmrC | - |
Escherichia coli |
Expression
| Organism | Comment | Expression |
|---|---|---|
| Salmonella enterica | expression of EptA (PmrC) is under the control of PmrA/PmrB | additional information |
| Escherichia coli | the peptA (eptA promoter) is induced sevenfold in the presence of Fe3+, induction is lost in enzyme mutant strain CH020 (DELTApmrA) | up |
General Information
| General Information | Comment | Organism |
|---|---|---|
| malfunction | although Salmonella lipid A is more prevalently modified with L-4-aminoarabinose, loss of Salmonella lpxT greatly increases modification of lipid A through enzyme EptA, and LpxT-dependent lipid A modification is not restored in the DELTAeptA mutant. LpxT catalyses the phosphorylation of lipid A at the 1-position forming 1-diphosphate lipid A increasing the negative charge of the bacterial surface | Salmonella enterica |
| malfunction | eptA mutants show a 20fold decrease in polymyxin B resistanc. Overexpression of LpxT in trans in Escherichia coli strain WD101 results in loss of phosphoethanolamine modification and compromised WD101 polymyxin resistance | Escherichia coli |
| metabolism | PmrA is activated under Mg2+ limiting growth conditions or upon exposure to cationic antimicrobial peptides. Under these conditions PmrA activation is mediated by a second two-component system, PhoP/PhoQ. activation of PhoP in Salmonella induces the synthesis of PmrD, which regulates PmrA activity post-transcriptionally by preventing dephosphorylation of PmrA | Salmonella enterica |
| physiological function | EptA-dependent lipid A modification is required for resistance to polymyxin B, EptA plays a dominant role in polymyxin resistance. Enzyme PmrA is not involved in transcription of LpxT, which catalyses the phosphorylation of lipid A at the 1-position forming 1-diphosphate lipid A increasing the negative charge of the bacterial surface. LpxT-dependent lipid A modification is regulated post-translationally. The regulation does not occur at the level of transcription, but rather following the assembly of LpxT into the inner membrane. PmrA-dependent inhibition of LpxT is required for phosphoethanolamine decoration of lipid A, which is critical for Escherichia coli to resist the bactericidal activity of polymyxin | Escherichia coli |
| physiological function | EptA-dependent lipid A modification is required for resistance to polymyxin B. Expression of EptA (PmrC) is under the control of PmrA/PmrB | Salmonella enterica |
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