Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.5.1.1 (asparaginase)
 2,695 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The complete genome of Acinetobacter oleivorans DR1 contains AqsR and AqsI genes, which are LuxR and LuxI homolog, respectively. In a previous study, we demonstrated that quorum sensing (QS) signals play an important role in biofilm formation and hexadecane biodegradation. However, the regulation of genes controlled by the QS system in DR1 remains unexplored. We constructed an aqsR mutant and performed RNA sequencing analysis to understand the QS system. A total of 353 genes were differentially expressed during the stationary phase of wild-type cells compared to that of the aqsR mutant. AqsR appears to be an exceptionally important regulator because knockout of aqsR affected global gene expression. Genes involved in posttranslational modification, chaperones, cell wall structure, secondary metabolites biosynthesis, and stress defense were highly upregulated only in the wild type. Among upregulated genes, both the AOLE_03905 (putative surface adhesion protein) and the AOLE_11355 (L-asparaginase) genes have putative LuxR binding sites at their promoter regions. Soluble AqsR proteins were successfully purified in Escherichia coli harboring both aqsR and aqsI. Comparison of QS signals in an AqsI-AqsR co-overexpression strain with N-acyl homoserine lactone standards showed that the cognate N-acyl homoserine lactone binding to AqsR might be 3OH C12HSL. Our electrophoretic mobility shift assays with purified AqsR revealed direct binding of AqsR to those promoter regions. Our data showed that AqsR functions as an important regulator and is associated with several phenotypes, such as hexadecane utilization, biofilm formation, and sensitivity to cumene hydroperoxide.
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PMID:Identification and characterization of genes regulated by AqsR, a LuxR-type regulator in Acinetobacter oleivorans DR1. 2374 19

Quorum sensing (QS)-dependent biofilm formation and motility were controlled by AqsR in Acinetobacter oleivorans DR1. QS-controlled phenotypes appeared to be inhibited by indole and the aqsR mutant had the same phenotypes. We demonstrated that the turnover rate of AqsR became more rapid without the N-acylhomoserine lactone (AHL) signal, and that indole could increase the expression of many protease and chaperone proteins. The addition of exogenous indole decreased the expression of two AqsR-targeted genes: AOLE_03905 (putative surface adhesion protein) and AOLE_11355 (L-asparaginase). The overexpression of AqsR in Escherichia coli was impossible with the indole treatment. Surprisingly, our [(35)S]methionine pulse-labelling data demonstrated that the stability and folding of AqsR protein decreased in the presence of indole without changing aqsR mRNA expression in E. coli. Interestingly, indole resulted in a loss of TraR-dependent traG expression in an Agrobacterium tumefaciens indicator strain. However, when indole was added after incubation with exogenous AHL, indole could not inhibit the TraR-dependent expression of the traG promoter. This indicated that AHL-bound TraR could be protective against indole, but TraR without AHL could not be active in the presence of indole. Here, we provided evidence for the first time showing that the indole effect on QS-controlled bacterial phenotypes is due to inhibited QS regulator folding and not a reduced QS signal.
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PMID:Indole inhibits bacterial quorum sensing signal transmission by interfering with quorum sensing regulator folding. 2402 5