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Published on February 23, 2007; 10.1104/pp.106.093294


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Received November 17, 2006
Accepted January 18, 2007

Mastoparan Activates Calcium Spiking Analogous to Nod Factor-induced Responses in Medicago truncatula Root hair cells

Jongho Sun , Hiroki Miwa , J. Allan Downie , and Giles E. D. Oldroyd *

Departments of Disease and Stress Biology and Molecular Microbiology, John Innes Centre, Norwich Research Park, Norwich NR4 7UH, UK

* Corresponding author; email: giles.oldroyd{at}bbsrc.ac.uk.

The rhizobial derived signalling molecule Nod factor is essential for the establishment of the Medicago truncatula/Sinorhizobium meliloti symbiosis. Nod factor perception and signal transduction in the plant involves calcium spiking and leads to the induction of nodulation gene expression. It has previously been shown that the heterotrimeric G-protein agonist mastoparan can activate nodulation gene expression in a manner analogous to Nod factor activation of these genes and this requires DMI3, a calcium and calmodulin dependent protein kinase (CCaMK) that is required for Nod factor signalling. Here we show that Mastoparan activates oscillations in cytosolic calcium, similar but not identical to Nod factor induced calcium spiking. Mastoparan induced calcium changes occur throughout the cell, whereas Nod factor induced changes are restricted to the region associated with the nucleus. Mastoparan induced calcium spiking occurs in plants mutated in the receptor-like kinases NFP and DMI2 and in the putative cation channel DMI1, that are all required for Nod factor induction of calcium spiking, indicating either that Mastoparan functions downstream of these components or that it uses an alternative mechanism to Nod factor for activation of calcium spiking. However, both Mastoparan and Nod factor induced calcium spiking are inhibited by cyclopiazonic acid and n-butanol, suggesting some common mechanisms underpinning these two calcium agonists. The fact that Mastoparan and Nod factor both activate calcium spiking and can induce nodulation gene expression in a DMI3 dependent manner strongly implicates CCaMK in the perception and transduction of the calcium signal.




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