| Mutant Symbol |
Allele or Genotype |
Mutant Gene |
Phenotype Detail |
Symbiotic Phenotype Brief |
Mutagenesis Method |
Mutant Class |
WT Strain or Line |
|---|
| latd | latd | latd | The latd mutant plants initiate nodule formation but do not complete it, resulting in immature, non-nitrogen-fixing nodules. The latd mutant nodules are small and white, consistent with a lack of full differentiation. Similarly, lateral roots initiate, but remain short stumps. The primary root, which initially appears to be wild type, gradually ceases growth and forms an abnormal tip that resembles that of the mutant lateral roots. The latd mutation causes disorganization of the primary root meristem, blocks root growth, blocks elongation of lateral roots and causes disorganization of the lateral root tip and reduces the length and density of root hairs. Infection by the rhizobial partner, Sinorhizobium meliloti, can occur, although infection is rarely completed. Once inside latd mutant nodules, S. meliloti fails to express rhizobial genes associated with the developmental transition from free-living bacterium to endosymbiont, such as bacA and nex38. The infecting rhizobia also fail to express nifH and fix nitrogen. Thus, both plant and bacterial development are blocked in latd mutant roots.
Liang et al. (2007) showed that the plant hormone, abscisic acid (ABA), can rescue the latd root, but not nodule, meristem defects. Growth on ABA is sufficient to restore formation of small, cytoplasm-rich cells in the presumptive meristem region, rescue meristem organization and root growth and formation of root cap columella cells. Their results demonstrated that latd mutant is defective in the ABA response. | Nod+Fix- | EMS | Nod+Fix- | Jemalong A17 |
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