| In a screen of Medicago truncatula Gaertn. plants for mutants with defects in the Rhizobium-legume symbiosis I identified one mutant, which made small Fix− nodules that contain abnormal infection threads. Infections aborted in the epidermis and outer cortical cells of the root, terminating with large accumulations of bacteria in the swollen ends of infection threads. This mutant also produces short root hairs and short, bent, blunt trichomes. Genetic analysis showed the three phenotypes are recessive and cosegregate; they segregate as a single locus. Because of the three phenotypes, I named the locus RIT1 for abnormal, root hairs, infection threads, and trichomes. Microscopic analysis of mutant nodules shows that many nodule cells contain centrally located cytoplasm, indicating activation of the cell cycle. Infection thread ultrastructural analysis in rit1 mutants shows bacteria are not released from infection threads, and bacteria inside mutant and wild type infections are similar in appearance. Expression analysis of genes associated with the symbiosis shows several are misregulated in the mutant.; In addition, I identified eight independent symbiotic mutants with defects in nitrogen fixation (Fix−). The eight Fix− mutants represent seven complementation groups. All mutants segregate as single loci with the exception of one, whose segregation suggests a single locus with incomplete penetrance of the Fix− phenotype. I have named these loci DNF1 to DNF7 (for d&barbelow;efective in n&barbelow;itrogen f&barbelow;ixation). Analysis of the Fix− mutants showed that early infection events by Sinorhizobium meliloti were normal. I also analyzed the mutants for their ability to induce bacterial symbiotic gene expression. Despite similarities in their nodulation phenotype these Fix− mutants differ in their ability to induce bacterial symbiotic genes. I classify the Fix− mutants into three groups that are defective at different stages in the interaction with the bacterial partner. |
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