Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 99, Issue 6, Pages 3938-3943Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.062425699
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- NIGMS NIH HHS [GM31030, R01 GM031030, T32 GM007287, T32GM07287] Funding Source: Medline
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Our analyses of lipopolysaccharide mutants of Sinorhizobium meliloti offer insights into how this bacterium establishes the chronic intracellular infection of plant cells that is necessary for its nitrogen-fixing symbiosis with alfalfa. Derivatives of S. meliloti !;train Rm1021 carrying an Ips8 mutation are capable of colonizing curled root hairs and forming infection threads in alfalfa in a manner similar to a wild-type strain. However, developmental abnormalities occur in the bacterium and the plant at the stage when the bacteria invade the plant nodule cells. Loss-of-function lpsE mutations, which eliminate a protein of the glycosyltransferase I family, cause striking changes in the carbohydrate core of the lipopolysaccharide, including the absence of uronic acids and a 40-fold relative increase in xylose. We also found that Ips8 mutants were sensitive to the cationic peptides melittin, polymyxin B, and poly-L-lysine, in a manner that paralleled that of Brucella abortus lipopolysaccharide mutants. Sensitivity to components of the plant's innate immune system may be part of the reason that this mutant is unable to properly sustain a chronic infection within the cells of its host-plant alfalfa.
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