Branching in Pea (Action of Genes Rms3 and Rms4)

Abstract

The nonallelic ramosus mutations rms3-2 and rms4 of pea (Pisum safivum 1.) cause extensive release of vegetative axillary buds and lateral growth in comparison with wild-type (cv Torsdag) plants, i n which axillary buds are not normally released under the conditions utilized. Crafting studies showed that the expression of the rms4 mutation i n the shoot is independent of the genotype of the rootstock. I n contrast, the length of the branches at certain nodes of rms3-2 plants was reduced by grafting to wild-type stocks, indicating that the wild-type Rms3 gene may control the level of a mobile substance produced in the root. This substance also appears to be produced in the shoot because Rms3 shoots did not branch when grafted to mutant rms3-2 rootstocks. However, the end product of 953-959) because reciproca1 grafts between rms3-2 and rms2 seedlings produced mature shoots with apical dominance similar to that of rms3-2 and rms2 shoots grafted to wild-type stocks. Indole-3-acetic acid levels were not reduced in apical or nodal portions of rms4 plants and were actually elevated (up t o 2-fold) in rms3-2 plants. It is suggested that further studies with these branching mutants may enable significant progress in understanding the normal control of apical dominance and the related communication between the root and shoot.

Strigolactones fine-tune the root system

“…Some studies have demonstrated that in the strigolactone mutants the auxin levels were higher (Beveridge et al 1997b;Bennett et al 2006) whereas others that the mutants and the wild type did not differ (Beveridge et al 1996;Morris et al 2001;Arite et al 2009). There is also support for a role of strigolactones in reducing polar auxin transport both by means of radiolabeled auxins and PIN efflux marker lines, although contradictory results concerning subcellular relocalisation of PINs in root tips have been reported in different experiments and when the root and shoot systems were compared (Beveridge et al 2000;Bennett et al 2006;Lazar and Goodman 2006;Lin et al 2009;Crawford et al 2010;Shinohara et al 2013).…”

“…Auxin is also regulated by positive feedback loops between biosynthesis and transport, so the higher levels of auxin biosynthesis may cause the higher levels of transporter proteins observed in primary roots (Ruyter-Spira et al 2011) and also the higher levels of auxin measured at the bases of cuttings from tomato strigolactone mutants . Opposing evidence for this theory is that the strigolactone mutants of pea do not necessarily have a higher auxin content than that of the wild type (Beveridge et al 1996;Morris et al 2001). Additional proof against strigolactone directly regulating auxin biosynthesis is found in root hair lengths, where exogenous treatments with auxins using the PIN efflux pathway were unable to restore the phenotype (Koltai et al 2010), suggesting a more direct interaction with the PIN pathway.…”

“…Yet, early studies already reported that strigolactone shoot branching mutants in pea and petunia had reduced root biomass (Beveridge et al 1996;Snowden et al 2005;Drummond et al 2009) whereas the dry weight of other strigolactone mutants did not differ from the wild type (Beveridge et al 1997a;Morris et al 2001). In petunia strigolactone mutants, no obvious change in root structure associated with the observed reduction in root mass (Snowden et al 2005).…”

Strigolactone Acts Downstream of Auxin to Regulate Bud Outgrowth in Pea and Arabidopsis

“…In recent decades, many branching mutants have been isolated that have problems with auxin, cytokinin, or brassinosteroids, for example, and show highly pleiotropic phenotypes typical for these hormones (Lincoln et al, 1990;Azpiroz et al, 1998;Tantikanjana et al, 2001). However, a class of mutants were isolated that displayed a specific increase in bud outgrowth that was not correlated with any known hormonal signal (Beveridge et al, 1996(Beveridge et al, , 1997. Paradoxically, the mutants were found to have generally higher levels of auxin and lower levels of xylem cytokinin, facts difficult to reconcile with ideas about the roles of auxin and cytokinin in regulating bud outgrowth (Beveridge et al, 1997).…”

“…Mutant phenotypes were rescued by grafting with wild-type tissue, even in interstock grafts where small pieces of wild-type stem tissue were grafted between mutant rootstock and shoot tissue (Napoli, 1996;Foo et al, 2001). Other mutants were not rescued by grafting but were instead suggested to lack response to SMS (Beveridge et al, 1996;Booker et al, 2005). Grafting studies also showed that outgrowth induced by decapitation in SMS mutant plants cannot be inhibited by IAA applied to the stump unless a wild-type rootstock is present .…”