ABSTRACT
Rhizobial phosphatidylcholine (PC) is thought to be a critical phospholipid for the symbiotic relationship between rhizobia and legume host plants. A PC-deficient mutant of Sinorhizobium meliloti overproduces succinoglycan, is unable to swim, and lacks the ability to form nodules on alfalfa (Medicago sativa) host roots. Suppressor mutants had been obtained which did not overproduce succinoglycan and regained the ability to swim. Previously, we showed that point mutations leading to altered ExoS proteins can reverse the succinoglycan and swimming phenotypes of a PC-deficient mutant. Here, we report that other point mutations leading to altered ExoS, ChvI, FabA, or RpoH1 proteins also revert the succinoglycan and swimming phenotypes of PC-deficient mutants. Notably, the suppressor mutants also restore the ability to form nodule organs on alfalfa roots. However, nodules generated by these suppressor mutants express only low levels of an early nodulin, do not induce leghemoglobin transcript accumulation, thus remain white, and are unable to fix nitrogen. Among these suppressor mutants, we detected a reduced function mutant of the 3-hydoxydecanoyl-acyl carrier protein dehydratase FabA that produces reduced amounts of unsaturated and increased amounts of shorter chain fatty acids. This alteration of fatty acid composition probably affects lipid packing thereby partially compensating for the previous loss of PC and contributing to the restoration of membrane homeostasis.
Subject(s)
Fatty Acids , Medicago sativa , Phosphatidylcholines , Plant Root Nodulation , Sinorhizobium meliloti , Symbiosis , Sinorhizobium meliloti/physiology , Sinorhizobium meliloti/genetics , Medicago sativa/microbiology , Medicago sativa/genetics , Plant Root Nodulation/genetics , Fatty Acids/metabolism , Fatty Acids/biosynthesis , Phosphatidylcholines/metabolism , Phosphatidylcholines/biosynthesis , Bacterial Proteins/genetics , Bacterial Proteins/metabolism , Root Nodules, Plant/microbiology , Root Nodules, Plant/genetics , Root Nodules, Plant/metabolism , Mutation , Polysaccharides, Bacterial/metabolism , Polysaccharides, Bacterial/biosynthesis , Nitrogen FixationABSTRACT
Phosphorus (P) availability is a limiting factor for plant growth and development. Root tip contact with low Pi media triggers diverse changes in the root architecture of Arabidopsis thaliana. The most conspicuous among these modifications is the inhibition of root growth, which is triggered by a shift from an indeterminate to a determinate root growth program. This phenomenon takes place in the root tip and involves a reduction in cell elongation, a decrease in cell proliferation, and the induction of premature cell differentiation, resulting in meristem exhaustion. Here, we review recent findings in the root response of A. thaliana to low Pi availability and discuss the cellular and genetic basis of the inhibition of root growth in Pi-deprived seedlings.
