1. Laboratory of Gene Expression, Department of Molecular Biology, University of Aarhus, Gustav Wieds Vej 10, DK-8000 Aarhus C, Denmark
2. National Institute of Agrobiological Sciences, Kannon-dai, Tsukuba, Ibaraki 305-8602, Japan
3. University of Munich, Department of Biology I, Genetics, Maria-Ward-Strasse 1a, D-80638 München, Germany
4. John Innes Centre, Colney, Norwich NR4 7UH, UK
5. University of Tokyo, Department of Biological Sciences, Graduate School of Science, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan
6. Kazusa DNA Research Institute, Kisarazu, Chiba, 292-0818, Japan

Correspondence to: Jens Stougaard¹ Correspondence and requests for materials should be addressed to J.S (Email: stougaard@mb.au.dk). The sequences for the L. japonicus ecotype GIFU CCaMK gene and mRNA are deposited in the EMBL nucleotide database under accession numbers AM230792 and AM230793.

Abstract

Induced development of a new plant organ in response to rhizobia is the most prominent manifestation of legume root-nodule symbiosis with nitrogen-fixing bacteria. Here we show that the complex root-nodule organogenic programme can be genetically deregulated to trigger de novo nodule formation in the absence of rhizobia or exogenous rhizobial signals. In an ethylmethane sulphonate-induced snf1 (spontaneous nodule formation) mutant of Lotus japonicus, a single amino-acid replacement in a Ca²⁺/calmodulin-dependent protein kinase (CCaMK) is sufficient to turn fully differentiated root cortical cells into meristematic founder cells of root nodule primordia. These spontaneous nodules are genuine nodules with an ontogeny similar to that of rhizobial-induced root nodules, corroborating previous physiological studies¹. Using two receptor-deficient genetic backgrounds we provide evidence for a developmentally integrated spontaneous nodulation process that is independent of lipochitin–oligosaccharide signal perception and oscillations in Ca²⁺ second messenger levels. Our results reveal a key regulatory position of CCaMK upstream of all components required for cell-cycle activation, and a phenotypically divergent series of mutant alleles demonstrates positive and negative regulation of the process.

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