Chronic intracellular infection of alfalfa nodules by Sinorhizobium meliloti requires correct lipopolysaccharide core

Abstract

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 strain Rm1021 carrying an lpsB 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 lpsB 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 lpsB 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.

How rhizobial symbionts invade plants: the Sinorhizobium–Medicago model

“…The lpsB mutant symbiotic defect is probably a result of its compromised outer membrane; however, as these bacteria also appear to lack contact with the plant symbiosome membrane, it is possible that they fail to survive because they cannot interact properly with the host 82 . figure) and the Brucella abortus pmm mutant produces a truncated LPS core 82,160,161 . Neither mutant can survive within host cells and this might be because their outer membranes are compromised 82,160 .…”

“…LPS consists of a lipid A membrane anchor attached to a polysaccharide core that in turn is attached to an O-antigen repeating unit 82 . The S. meliloti bacA gene is required by S. meliloti for the production of lipid A of the appropriate structure and for survival within host cells 83,84 …”

“…Although it can invade the plant root, become enclosed within a symbiosome membrane and begin to elongate into the bacteroid form, it cannot complete the bacteroid differentiation programme and fix nitrogen 82 . The lpsB mutant symbiotic defect is probably a result of its compromised outer membrane; however, as these bacteria also appear to lack contact with the plant symbiosome membrane, it is possible that they fail to survive because they cannot interact properly with the host 82 .…”

“…and S. meliloti within host cells. The S. meliloti lpsB mutant produces an LPS core with altered sugar composition (see figure) and the Brucella abortus pmm mutant produces a truncated LPS core 82,160,161 . Neither mutant can survive within host cells and this might be because their outer membranes are compromised 82,160 .…”

“…figure) and the Brucella abortus pmm mutant produces a truncated LPS core 82,160,161 . Neither mutant can survive within host cells and this might be because their outer membranes are compromised 82,160 . These mutants are also sensitive to detergents and to antimicrobial peptides, such as polymyxin B, that resemble defence compounds produced by phagocytic cells and plant cells 82,162,163 .…”