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Background  Soil bacteria collectively known as  Rhizobium , characterized by their ability to establish beneficial symbiosis with legumes, share several common characteristics with pathogenic bacteria when infecting the host plant. Recently, it was demonstrated that a  fadD  mutant of  Sinorhizobium meliloti  is altered in the control of swarming, a type of co-ordinated movement previously associated with pathogenicity, and is also impaired in nodulation efficiency on alfalfa roots. In the phytopathogen  Xanthomonas campestris , a  fadD  homolog ( rpfB ) forms part of a cluster of genes involved in the  r egulation of  p athogenicity  f actors. In this work, we have investigated the role in swarming and symbiosis of SMc02161, a  S. meliloti fadD -linked gene.    Results  The SMc02161 locus in  S. meliloti  shows similarities with members of the Major Facilitator Superfamily (MFS) of transporters. A  S. meliloti  null-mutant shows increased sensitivity to chloramphenicol. This indication led us to rename the locus  tep1  for  t ransmembrane  e fflux  p rotein. The lack of  tep1  does not affect the appearance of swarming motility. Interestingly, nodule formation efficiency on alfalfa plants is improved in the  tep1  mutant during the first days of the interaction though  nod  gene expression is lower than in the wild type strain. Curiously, a  nodC  mutation or the addition of  N -acetyl glucosamine to the wild type strain lead to similar reductions in  nod  gene expression as in the  tep1  mutant. Moreover, aminosugar precursors of Nod factors inhibit nodulation.    Conclusion   tep1  putatively encodes a transmembrane protein which can confer chloramphenicol resistance in  S. meliloti  by expelling the antibiotic outside the bacteria. The improved nodulation of alfalfa but reduced  nod  gene expression observed in the  tep1  mutant suggests that Tep1 transports compounds which influence nodulation. In contrast to  Bradyrhizobium japonicum , we show that in  S. meliloti  there is no feedback regulation of nodulation genes. Moreover, the Nod factor precursor,  N -acetyl glucosamine reduces  nod  gene expression and nodulation efficiency when present at millimolar concentrations. A role for Tep1 in the efflux of Nod factor precursors could explain the phenotypes associated with  tep1  inactivation.

bmc microbiology

The tep1 gene of Sinorhizobium meliloti coding for a putative transmembrane efflux protein and N-acetyl glucosamine affect nod gene expression and nodulation of alfalfa plants