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

The ramosus (rms) mutation (rms1) of pea (Pisum sativum) causes increased b ranching 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 Rms1 moves acropetally in shoots and act s as a branching inhibitor. Epicotyl interstock grafts showed that wild-typ e (WT) epicotyls grafted between rms1 scions and rootstocks can revert muta nt scions to a WT non-branching phenotype. Mutant scions grafted together w ith mutant and WT rootstocks did not branch despite a contiguous mutant roo t-shoot system. The primary action of Rms1 is, therefore, unlikely to be to block transport of a branching stimulus from root to shoot. Rather, Rms1 m ay influence a long-distance signal that functions, directly or indirectly, as a branching inhibitor. It can be deduced that this signal moves acropet ally in shoots because WT rootstocks inhibit branching in rms1 shoots, and although WT scions do not branch when grafted to mutant rootstocks, they do not inhibit branching in rms1 cotyledonary shoots growing from the same ro otstocks. The acropetal direction of transport of the Rms1 signal supports previous evidence that the rms1 lesion is not in an auxin biosynthesis or t ransport pathway. The different branching phenotypes of WT and rms1 shoots growing from the same rms1 rootstock provides further evidence that the sho ot has a major role in the regulation of branching and, moreover, that root -exported cytokinin is not the only graft-transmissible signal regulating b ranching in intact pea plants.