Long-distance signaling and the control of branching in the rms1 mutant of pea

The <em>ramosus</em> (<em>rms</em>) mutation (<em>rms1</em>) of pea (<em>Pisum sativum</em>) causes increased branching through modification of graft-transmissible signal(s) produced in rootstock and shoot. Additional grafting techniques have led us to propose that the novel signal regulated by<em>Rms1</em> moves acropetally in shoots and acts as a branching inhibitor. Epicotyl interstock grafts showed that wild-type (WT) epicotyls grafted between <em>rms1</em> scions and rootstocks can revert mutant scions to a WT non-branching phenotype. Mutant scions grafted together with mutant and WT rootstocks did not branch despite a contiguous mutant root-shoot system. The primary action of<em>Rms1</em> is, therefore, unlikely to be to block transport of a branching stimulus from root to shoot. Rather, <em>Rms1</em>may influence a long-distance signal that functions, directly or indirectly, as a branching inhibitor. It can be deduced that this signal moves acropetally in shoots because WT rootstocks inhibit branching in <em>rms1</em> shoots, and although WT scions do not branch when grafted to mutant rootstocks, they do not inhibit branching in <em>rms1</em> cotyledonary shoots growing from the same rootstocks. The acropetal direction of transport of the<em>Rms1</em> signal supports previous evidence that the<em>rms1</em> lesion is not in an auxin biosynthesis or transport pathway. The different branching phenotypes of WT and<em>rms1</em> shoots growing from the same <em>rms1</em>rootstock provides further evidence that the shoot has a major role in the regulation of branching and, moreover, that root-exported cytokinin is not the only graft-transmissible signal regulating branching in intact pea plants.