Sinorhizobium meliloti forms symbiotic,
nitrogen-fixing nodules on the roots of Medicago truncatula. The bacteria invade and colonize the roots through structures called
infection threads. S. meliloti unable to produce the exopolysaccharide
succinoglycan are unable to establish a symbiosis because they are defective in initiating the production of
infection threads and in invading the plant. Here, we use microarrays representing 16,000 M. truncatula genes to compare the differential transcriptional responses of this host plant to wild-type and
succinoglycan-deficient S. meliloti at the early time point of 3 days postinoculation. This report describes an early divergence in global plant gene expression responses caused by a rhizobial defect in
succinoglycan production, rather than in Nod factor production. The microarray data show that M. truncatula inoculated with wild-type,
succinoglycan-producing S. meliloti more strongly express genes encoding translation components, protein degradation machinery, and some nodulins than plants inoculated with
succinoglycan-deficient bacteria. This finding is consistent with wild-type-inoculated plants having received a signal, distinct from the well characterized Nod factor, to alter their metabolic activity and prepare for invasion. In contrast, M. truncatula inoculated with
succinoglycan-deficient S. meliloti more strongly express an unexpectedly large number of genes in two categories: plant defense responses and unknown functions. One model consistent with our results is that appropriate symbiotically active exopolysaccharides act as signals to plant hosts to initiate
infection thread formation and that, in the absence of this signal, plants terminate the
infection process, perhaps via a defense response.