Results and Discussion

S. meliloti Rml021 usually produces succinoglycan but not EPS II. When growing in low phosphate media or carrying a null allele of the regulatory gene called mucR, Rml021 produces EPS II, but only high molecular weight (HMW) forms that are not active in symbiosis. A spontaneous mutation originally called expRlOl induces Rml021 to produce EPS II ranging from LMW to HMW, and so Rml021 expRlOl derivatives strains induce the formation of functional nodules even when they are deficient in succinoglycan production. We have found that expRlOl mutation is actually an insertion sequence excision, which restores the function of a gene, expR. The predicted product of expR shares homology with the LuxR transcriptional regulator family.

We have also studied the possible roles of another type of surface polysaccharide, the lipopolysaccharide, in symbiosis. We have identified a mutant named fix389 that presented a deficient phenotype after its release from the infection threads. The fix389 mutant, which carries a null allele of a putative glycosyl transferase encoded by the IpsB gene, has an altered LPS core and is more sensitive to several cationic peptides. The nodules formed by the IpsB mutant show several abnormalities, including plant cells containing large vacuoles and bacteroids with PHB granules. The plants infected by fix389 were much smaller than the control plants and exhibit nitrogen deficiency symptoms. We suggest that the mutant might be highly sensitive to plant's defense responses and is thus unable to establish a proper chronic infection within the plant cells.

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