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The Unphosphorylated EIIA.sup.Ntr Protein Represses the Synthesis of Alkylresorcinols in Azotobacter vinelandii

Upon encystment induction, Azotobacter vinelandii produces the phenolic lipids alkylresorcinols (ARs) that are structural components of the cysts. The enzymes responsible for the ARs synthesis are encoded in the arsABCD operon, whose expression is activated by ArpR. The transcription of arpR is init...

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Published in:PloS one 2015-02, Vol.10 (2), p.e0117184
Main Authors: Muriel-Millán, Luis Felipe, Moreno, Soledad, Romero, Yanet, Bedoya-Pérez, Leidy Patricia, Castañeda, Miguel, Segura, Daniel, Espín, Guadalupe
Format: Article
Language:English
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Summary:Upon encystment induction, Azotobacter vinelandii produces the phenolic lipids alkylresorcinols (ARs) that are structural components of the cysts. The enzymes responsible for the ARs synthesis are encoded in the arsABCD operon, whose expression is activated by ArpR. The transcription of arpR is initiated from an RpoS dependent promoter. The nitrogen-related phosphotransferase system (PTS.sup.Ntr) is a global regulatory system present in Gram negative bacteria. It comprises the EI.sup.Ntr, NPr and EIIA.sup.Ntr proteins encoded by ptsP, ptsO and ptsN genes respectively. These proteins participate in a phosphoryl-group transfer from phosphoenolpyruvate to protein EIIA.sup.Ntr via the phosphotransferases EI.sup.Ntr and NPr. In A. vinelandii, the non-phosphorylated form of EIIA.sup.Ntr was previously shown to repress the synthesis of poly-ß-hydroxybutyrate. In this work, we show that PTS.sup.Ntr also regulates the synthesis of ARs. In a strain that carries unphosphorylated EIIA.sup.Ntr, the expression of arpR was reduced, while synthesis of ARs and transcription of arsA were almost abrogated. The expression of arpR from an RpoS-independent promoter in this strain restored the ARs synthesis. Taken together these results indicate that unphosphorylated EIIA.sup.Ntr negatively affects activation of arpR transcription by RpoS.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0117184