| Mutant Symbol | dmi3-1 DMI3p-DMI3 1-311 |
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| Allele Symbol | dmi3-1 DMI3p-DMI3 1-311 |
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| Gene and Mutation Location | DMI3 (The CaM-binding domain and the remaining of DMI3 is deleted. Only first 311 aa of the protein were kept.) |
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| Symbiotic Phenotype Brief | Nod+Fix- |
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| Phenotype Detail | 43% of dmi3-1 plants (20 of 47) transformed with DMI3p-DMI3
1-311 showed spontaneous nodules, with an average of 5.4 nodules per plant. Spontaneous nodules induced by DMI3p-DMI3 1-311 showed appropriate ENOD11-GUS induction. When S. meliloti was inoculated onto dmi3-1 roots transformed with DMI3p-DMI3 1-311, no bacteria was detected inside the nodules and little indication of root hair responses and no development of infection threads was observed. Hence, even though DMI3p-DMI3 1-311 leads to the formation of nodules, it is not sufficient to fully complement the dmi3-1 mutation to allow bacterial entry. |
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| Single gene targeted? | yes |
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| Extra Information | The deletion in DMI3 1-311 leads to constitutive substrate phosphorylation in vitro that is independent of Ca2+ and CaM. The fact that DMI3 1-311 and DMI3 1-326 are able to induce nodules, but are not sufficient to allow bacterial entry, indicates essential roles for the CaM-binding and EF-hand domains during rhizobial infection. It is possible that although the simple release of autoinhibition is sufficient to induce nodule development, the appropriate spatial and temporal activation of CCaMK might be required during bacterial infection. |
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| Mutagenesis Method | deletion |
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| Mutant Class | Nod+Fix- |
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| Allelism | |
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| The earliest development stage known to be affected | N/A |
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| Wildtype Line | Jemalong J5 |
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