Mapping the Sinorhizobium meliloti 1021 solute-binding protein-dependent transportome

The number of solute-binding protein-dependent transporters in rhizobia is dramatically increased compared with the majority of other bacteria so far sequenced. This increase may be due to the high affinity of solute-binding proteins for solutes, permitting the acquisition of a broad range of growth...

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Published inProceedings of the National Academy of Sciences - PNAS Vol. 103; no. 47; pp. 17933 - 17938
Main Authors Mauchline, T.H, Fowler, J.E, East, A.K, Sartor, A.L, Zaheer, R, Hosie, A.H.F, Poole, P.S, Finan, T.M
Format Journal Article
LanguageEnglish
Published United States National Academy of Sciences 21.11.2006
National Acad Sciences
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Summary:The number of solute-binding protein-dependent transporters in rhizobia is dramatically increased compared with the majority of other bacteria so far sequenced. This increase may be due to the high affinity of solute-binding proteins for solutes, permitting the acquisition of a broad range of growth-limiting nutrients from soil and the rhizosphere. The transcriptional induction of these transporters was studied by creating a suite of plasmid and integrated fusions to nearly all ATP-binding cassette (ABC) and tripartite ATP-independent periplasmic (TRAP) transporters of Sinorhizobium meliloti. In total, specific inducers were identified for 76 transport systems, amounting to approximately equal to 47% of the ABC uptake systems and 53% of the TRAP transporters in S. meliloti. Of these transport systems, 64 are previously uncharacterized in Rhizobia and 24 were induced by solutes not known to be transported by ABC- or TRAP-uptake systems in any organism. This study provides a global expression map of one of the largest transporter families (transportome) and an invaluable tool to both understand their solute specificity and the relationships between members of large paralogous families.
Bibliography:http://dx.doi.org/10.1073/pnas.0606673103
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Edited by Eugene W. Nester, University of Washington, Seattle, WA, and approved October 1, 2006
Department of Microbiology, King's College London Dental Institute, Floor 28, Guy's Tower, Guy's Campus, London SE1 9RT, United Kingdom.
Author contributions: T.H.M. and J.E.F. contributed equally to this work; T.H.M., J.E.F., A.K.E., A.L.S., A.H.F.H., P.S.P., and T.M.F. designed research; T.H.M., J.E.F., A.L.S., and R.Z. performed research; T.H.M., J.E.F., A.K.E., A.L.S., P.S.P., and T.M.F. analyzed data; and T.H.M., J.E.F., A.K.E., P.S.P., and T.M.F. wrote the paper.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.0606673103