The L2 β-lactamase gene of Stenotrophomonas maltophilia has been shown to be involved in resistance of the β-lactams and its expression is regulated by the ampR gene, which divergently locates upstream of the L2 gene. In this study, L2 and its downstream gene, ampH, has been shown to be an operon as revealed by Quantitative Real-Time PCR (QRT-PCR), Reverse Transcriptase-PCR (RT-PCT), and chromosomal transcriptional fusion assay. The expression of ampH gene depends on the ampR-regulated L2 promoter (PL2) and its own promoter (PampH). The ampH gene previously annotated as a putative Na+/H+ antiporter in the genome project of S. maltophilia was found to be less involved in the sodium homeostasis, but more prominent in the regulation of the induction of L1 and L2 β-lactamase genes. The role of AmpH protein in the regulation of L1 and L2 genes induction is does-dependent. The induction of L1 gene in the absence of the AmpH protein proceeds to fewer extents, indicating the optimal L1 induction occurs with the support of sufficient AmpH. In contrast, the presence of surplus AmpH protein reduces the induction of L2 gene, while hardly influences the induction of L1 gene. Consequently, the optimal L1 and L2 induction is exquisitely controlled by an appropriate amount of AmpH protein, which may be cleverly administered by the down-regulated L2-ampH operon.
