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Predicted ATP-binding cassette systems in the phytopathogenic mollicute Spiroplasma kunkelii

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Abstract

Spiroplasma kunkelii is a cell wall-free, helical, and motile mycoplasma-like organism that causes corn stunt disease in maize. The bacterium has a compact genome with a gene set approaching the minimal complement necessary for cellular life and pathogenesis. A set of 21 ATP-binding cassette (ABC) domains was identified during the annotation of a draft S. kunkelii genome sequence. These 21 ABC domains are present in 18 predicted proteins, and are components of 16 functional systems, which account for 5% of the protein coding capacity of the S. kunkelii genome. Of the 16 systems, 11 are membrane-bound transporters, and two are cytosolic systems involved in DNA repair and the oxidative stress response; the genes for the remaining three hypothetical systems harbor nonsense and/or frameshift mutations, so their functional status is doubtful. Assembly of the 11 multicomponent transporters, and comparisons with other known systems permitted functional predictions for the S. kunkelii ABC transporter systems. These transporters convey a wide variety of substrates, and are critical for nutrient uptake, multidrug resistance, and perhaps virulence. Our findings provide a framework for functional characterization of the ABC systems in S. kunkelii.

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Acknowledgements

This project was supported in part by a Specific Cooperative Agreement (1275-22000-144-02) between the University of Oklahoma and the USDA-Agricultural Research Service. For the latest S. kunkelii genome sequencing data, visit ACGT’s website at http://www.genome.ou.edu/spiro.html. We gratefully acknowledge Ellen L. Dally for her excellent technical support. The work has been carried out in compliance with the current laws governing genetic experimentation in the USA.

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Correspondence to R. E. Davis.

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Communicated by W. Goebel

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Zhao, Y., Wang, H., Hammond, R.W. et al. Predicted ATP-binding cassette systems in the phytopathogenic mollicute Spiroplasma kunkelii . Mol Genet Genomics 271, 325–338 (2004). https://doi.org/10.1007/s00438-004-0983-y

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