[Show abstract][Hide abstract] ABSTRACT: Members of the Rhizobiaceae contain 27-hydroxyoctacosanoic acid (27OHC28:0) in their lipid A. A Rhizobium leguminosarum 3841 acpXL mutant (named here Rlv22) lacking a functional specialized acyl carrier lacked 27OHC28:0 in its lipid A, had altered growth and physiological properties (e.g., it was unable to grow in the presence of an elevated
salt concentration [0.5% NaCl]), and formed irregularly shaped bacteroids, and the synchronous division of this mutant and
the host plant-derived symbiosome membrane was disrupted. In spite of these defects, the mutant was able to persist within
the root nodule cells and eventually form, albeit inefficiently, nitrogen-fixing bacteroids. This result suggested that while
it is in a host root nodule, the mutant may have some mechanism by which it adapts to the loss of 27OHC28:0 from its lipid A. In order to further define the function of this fatty acyl residue, it was necessary to examine the lipid
A isolated from mutant bacteroids. In this report we show that addition of 27OHC28:0 to the lipid A of Rlv22 lipopolysaccharides is partially restored in Rlv22 acpXL mutant bacteroids. We hypothesize that R. leguminosarum bv. viciae 3841 contains an alternate mechanism (e.g., another acp gene) for the synthesis of 27OHC28:0, which is activated when the bacteria are in the nodule environment, and that it is this alternative mechanism which functionally
replaces acpXL and is responsible for the synthesis of 27OHC28:0-containing lipid A in the Rlv22 acpXL bacteroids.
Full-text · Article · Apr 2006 · Journal of Bacteriology