Conclusions Previous studies have demonstrated that the ability of certain bacteria to synthesize, accumulate and metabolize intracellular PHB stores is important in enhancing their capacity to survive unfavourable growth conditions [34–37]. Rhizobia in the soil environment must contend with varying nutrient conditions, from the carbon-deficient bulk soil, to the carbon-rich rhizosphere

[33]. The LDN-193189 in vitro ability to accumulate and utilize carbon stores would be highly advantageous, allowing rhizobia to cope with fluctuating carbon conditions, and thus, make them more competitive against other bacterial populations [38]. Previous studies have shown that mutant strains of S. meliloti unable to synthesize (phaC) or degrade (bdhA) PHB show a significant reduction in competitiveness for nodule occupancy PCI-32765 molecular weight [28, 39], with AS1842856 purchase mutants that are unable to synthesize PHB exhibiting a much greater loss in competitiveness

than those unable to degrade PHB [28], as we have confirmed here. This is the first study in which the competitiveness of an S. meliloti phaZ mutant has been investigated. It was expected, based upon the phenotype of the bdhA mutant [28], that the phaZ mutant would exhibit reduced nodulation competitiveness. Interestingly, the phaZ mutant was as competitive as wild-type in co-inoculation experiments, and consistently out-competed both phaC and bdhA mutants (Table 4). Studies in Azotobacter vinelandii have demonstrated a role for PHB in protection of the cell against environmental stresses including pH, oxidative

stress and UV damage [40]. It is conceivable that the enhanced competitiveness of the phaZ mutant, relative to the phaC and bdhA mutants, is due to an enhanced ability to tolerate the conditions encountered in the soil and rhizosphere as a result of the increased cytoplasmic PHB concentration. Interestingly, the phaZ mutant shows a similar reduction Benzatropine in long-term survival during starvation to the phaC mutant (Figure 1). This suggests that the inability to degrade PHB is just as detrimental to the cells as the inability to accumulate it. This also confirms that PHB degradation does play a significant role in fuelling cellular metabolism under adverse conditions, and that glycogen synthesis and degradation is not able to replace the function of PHB metabolism under these conditions. Previous studies have shown that S. meliloti mutants defective in PHB synthesis also exhibit a significant reduction in succinoglycan production under conditions favouring both succinoglycan and PHB production [41], suggesting that these pathways share a common regulatory factor. S. meliloti phaB and phaC mutants exhibit non-mucoid colony morphology on carbon-rich media, while bdhA mutants show a mucoid colony morphology.