Auxin inhibition of decapitation-induced branching is dependent on graft-transmissible signals regulated by genes rms1 and rms2

Decapitation-induced axillary bud outgrowth is a vital mechanism whereby sh oots are able to continue normal growth and development. In many plants, in cluding wild-type garden pea (Pisum sativum L.), this process can be inhibi ted by exogenous auxin. Using the ramosus (rms) increased branching mutants of pea, we present evidence that this response to auxin is dependent on gr aft-transmissible substance(s) regulated by the genes Rms1 and Rms2. The re sponse to exogenous auxin is massively diminished in decapitated rms1 and r ms2 mutant plants. However, basipetal auxin transport is not reduced in int act or decapitated mutants. Grafting rms1 or rms2 shoots onto wild-type roo tstocks restored the auxin response, indicating that Rms1 and Rms2 gene act ion in the rootstock is sufficient to enable an auxin response in mutant sh oots. We conclude that Rms1 and Rms2 act in the rootstock and shoot to cont rol levels of mobile substance(s) that interact with exogenous auxin in the inhibition of bud outgrowth after decapitation. At least for rms1, the red uced auxin response is unlikely to be due to an inability of auxin to decre ase xylem sap cytokinin content, as this is already low in intact rms1 plan ts. Consequently, we have genetic evidence that auxin action in decapitated plants depends on at least one novel long-distance signal.