Abstract
A mutagenesis program using ethylmethane sulfonate on Medicago truncatula Gaertn cv Jemalong, an annual, autogamous and diploid lucerne, permitted the isolation of a mutant (TE7) unable to establish an effective nitrogen-fixing symbiosis, [Nod+Fix-], with Rhizobium meliloti wild-type strains. The mutant phenotype is characterized by an altered infection process that leads to the formation of two kinds of inefficient nodules on the same root system. A certain proportion of the nodules are small, round, and uninfected, with infection threads limited to the outer root cortical cells. Others develop to a normal elongated shape and are infected; bacterial release occurs but the bacteria do not differentiate into bacteroids. The ratio of invaded to uninvaded nodules depends on the bacterial strain used. Throughout the infection process, certain events correlated with the plant defense response against pathogens can be observed: (a) the presence of polyphenolic compounds associated with the walls of infected cells and also with some parts of infection threads in the root cortex; (b) appositions on infection thread walls during the early stage of infection and also within the central tissue of infected nodules; and (c) autophagy of the plant cells that contain released bacteria. Genetic data suggest that the phenotype of TE7 is under monogenic and recessive control; this gene has been designated Mtsym1.