Interstrain competition and host control of nodulation in the Phaseolus vulgaris-Rhizobium leguminosarum bv. phaseoli symbiosis

Abstract

The legume-Rhizobium symbiosis is a plant-microbe interaction that results in the formation of nitrogen-fixing root nodules. Competition for nodulation among rhizobial strains is a significant, but poorly understood, ecological and agronomic problem. This study addressed the role of the host as a variable that may influence the outcome of interstrain competition. The Phaseolus vulgaris-Rhizobium leguminosarum bv. phaseoli symbiosis was studied to characterize the competitiveness of rhizobial strains and to correlate competitiveness with the ability to induce suppression, a host-mediated regulatory response that restricts the extent of nodulation. The results of this study showed that Rhizobium leguminosarum bv. phaseoli strains have differential intrinsic competitive abilities. There was a correspondence between competitiveness and effectiveness, but there was no correlation between competitiveness and nodulation characteristics. Two highly competitive and highly effective strains, TAL 1472 and TAL 182, were identified as good model strains for genetic manipulation. Nodulation in common bean was subject to nodulation suppression. When a primary inoculation was done on one side of a split-root, followed by a secondary inoculation on the opposite side with increasing delay, secondary nodulation was suppressed in a time-dependent manner, becoming more pronounced as the delay period was increased. strains with varying competitive abilities induced a suppression response that partially corresponded with their competitive abilities. suppressiveness was not related to the speed of nodule formation or to the nodulating potential of a strain. suppression was correlated with rhizobial presence inside the nodules, but was not related to the ability to induce visible nodule primordia, or to the ability to fix nitrogen. Homologous complementation restored the nodulation abilities of the nonnodulating Class I and the nodule primordia-forming Class II mutants. However, the complemented Class I mutants were ineffective and did not regain full ability to induce nodulation suppression. In contrast, the complemented Class II mutants regained the wild-type nodulation, fixation, and suppression characteristics. Restriction analysis of the cosmids complementing Class I mutants showed a 7.2-kb region in common. Two complementation groups corrected the Class II mutants (MLC35 and MLC640), showing an 8.0-kb and a 13.4-kb region in common, respectively.