The fifth increased branching ramosus (rms) mutant, rms5, from pea (Pisum sativum), is described here for phenotype and grafting responses with four other rms mutants. Xylem sap zeatin riboside concentration and shoot auxin levels in rms5 plants have also been compared with rms1 and wild type (WT). Rms1 and Rms5 appear to act closely at the biochemical or cellular level to control branching, because branching was inhibited in reciprocal epicotyl grafts between rms5 or rms1 and WT plants, but not inhibited in reciprocal grafts between rms5 and rms1 seedlings. The weakly transgressive or slightly additive phenotype of the rms1 rms5 double mutant provides further evidence for this interaction. Like rms1, rms5 rootstocks have reduced xylem sap cytokinin concentrations, and rms5 shoots do not appear deficient in indole-3-acetic acid or 4-chloroindole-3-acetic acid. Rms1 and Rms5 are similar in their interaction with other Rms genes. Reciprocal grafting studies with rms1, rms2, and rms5, together with the fact that root xylem sap cytokinin concentrations are reduced in rms1 and rms5 and elevated in rms2 plants, indicates that Rms1 and Rms5 may control a different pathway than that controlled by Rms2. Our studies indicate that Rms1 and Rms5 may regulate a novel graft-transmissible signal involved in the control of branching.

One of the first and most enduring roles identified for the plant hormone auxin is the mediation of apical dominance. Many reports have claimed that reduced stem indole-3-acetic acid (IAA) levels and/or reduced basipetal IAA transport directly or indirectly initiate bud growth in decapitated plants. We have tested whether auxin inhibits the initial stage of bud release, or subsequent stages, in garden pea (Pisum sativum) by providing a rigorous examination of the dynamics of auxin level, auxin transport, and axillary bud growth. We demonstrate that after decapitation, initial bud growth occurs prior to changes in IAA level or transport in surrounding stem tissue and is not prevented by an acropetal supply of exogenous auxin. We also show that auxin transport inhibitors cause a similar auxin depletion as decapitation, but do not stimulate bud growth within our experimental time-frame. These results indicate that decapitation may trigger initial bud growth via an auxin-independent mechanism. We propose that auxin operates after this initial stage, mediating apical dominance via autoregulation of buds that are already in transition toward sustained growth.Decapitated garden pea (Pisum sativum) seedlings, bearing axillary buds in leaf axils separated by long internodes, were one of the first systems used to study apical dominance in plants (Snow, 1931). In pea, several axillary buds respond to decapitation by enlarging, but only a few of these reach sustained growth; dormancy remains imposed or is reimposed in the remainder (Stafstrom and Sussex, 1988). This autoregulation of shoot branching is achieved by longdistance signaling (for review, see Napoli et al., 1999). The transition of axillary buds from dormancy to sustained growth in vegetative shoots involves several developmental stages typified by expression of particular molecular markers (Stafstrom and Sussex, 1988;Napoli et al., 1999;Shimizu-Sato and Mori, 2001). The action of long-distance signals at any one or more of these stages could mediate apical dominance.It is well known that the application of auxin to the stump of decapitated plants inhibits axillary bud outgrowth, although less is known about the stage at which auxin acts. A frequently overlooked feature of this inhibition is that it is rarely complete with axillary buds usually growing a small but measurable amount prior to or during inhibition. The results of experiments with auxin transport inhibitors also appear to be consistent with a key role for auxin in apical dominance. These compounds are reported to promote lateral outgrowth (naphthylphtalamic acid [NPA], Tamas, 1987; 2,3,5-triiodobenzoic acid [TIBA], Panigrahi and Audus, 1966; for review, see Shimizu-Sato and Mori, 2001). In the 1930s, studies of bud outgrowth in plants with two decapitated shoots led Snow (1937) to suggest that auxin inhibits branching via a second messenger moving acropetally. Using radiolabeled indole-3-acetic acid (IAA), Hall and Hillman (1975) also proposed that auxin acts indirectly. Auxin was shown to move predo...

Increased-branching mutants of garden pea (Pisum sativum; ramosus [rms]) and Arabidopsis (Arabidopsis thaliana; more axillary branches) were used to investigate control of cytokinin export from roots in relation to shoot branching. In particular, we tested the hypothesis that regulation of xylem sap cytokinin is dependent on a long-distance feedback signal moving from shoot to root. With the exception of rms2, branching mutants from both species had greatly reduced amounts of the major cytokinins zeatin riboside, zeatin, and isopentenyl adenosine in xylem sap compared with wild-type plants. Reciprocally grafted mutant and wild-type Arabidopsis plants gave similar results to those observed previously in pea, with xylem sap cytokinin downregulated in all graft combinations possessing branched shoots, regardless of root genotype. This long-distance feedback mechanism thus appears to be conserved between pea and Arabidopsis. Experiments with grafted pea plants bearing two shoots of the same or different genotype revealed that regulation of root cytokinin export is probably mediated by an inhibitory signal. Moreover, the signaling mechanism appears independent of the number of growing axillary shoots because a suppressed axillary meristem mutation that prevents axillary meristem development at most nodes did not abolish long-distance regulation of root cytokinin export in rms4 plants. Based on double mutant and grafting experiments, we conclude that RMS2 is essential for long-distance feedback regulation of cytokinin export from roots. Finally, the startling disconnection between cytokinin content of xylem sap and shoot tissues of various rms mutants indicates that shoots possess powerful homeostatic mechanisms for regulation of cytokinin levels.

We examined the role of cytokinins (CKs) in release of apical dominance in lateral buds of chickpea (Cicer arietinum L.). Shoot decapitation or application of CKs (benzyladenine, zeatin or dihydrozeatin) stimulated rapid bud growth. Time-lapse video recording revealed growth initiation within 2 h of application of 200 pmol benzyladenine or within 3 h of decapitation. Endogenous CK content in buds changed little in the ®rst 2 h after shoot decapitation, but signi®cantly increased by 6 h, somewhat later than the initiation of bud growth. The main elevated CK was zeatin riboside, whose content per bud increased 7-fold by 6 h and 25-fold by 24 h. Lesser changes were found in amounts of zeatin and isopentenyl adenine CKs. We have yet to distinguish whether these CKs are imported from the roots via the xylem stream or are synthesised in situ in the buds, but CKs may be part of an endogenous signal involved in lateral bud growth stimulation following shoot decapitation. To our knowledge, this is the ®rst detailed report of CK levels in buds themselves during release of apical dominance.Abbreviations: BA = N 6 -benzyladenine; CK = cytokinin; cv = cultivar; DHZ = dihydrozeatin; IP = isopentenyl adenine; IPA = isopentenyl adenosine; Z = zeatin; ZR = zeatin riboside

Treatment of children with swallowing dysfunction requires a holistic approach based on a global view of their problems and needs. The connection of the swallowing mechanism with the sensorimotor organization of postural tone and movement throughout the body is a critical factor in the evaluation and treatment of children whose dysphagia is rooted in a neurologic disorder. An appropriate program includes work with the development of movement skills, sensory processing, learning, social skills, and communication. The initial focus is placed on oral-motor treatment, rather than direct work on oral feeding. The primary goal of the program is to develop the appropriate use of the mouth, respiratory, and phonatory systems in exploration, sound play, and as much oral feeding as possible. Oral feeding is the by-product of a total program, not its major goal.

Our studies on two branching mutants of pea (Pisum sativum L.) have identified a further Ramosus locus, Rms6, with two recessive or partially recessive mutant alleles: rms6-1 (type line S2-271) and rms6-2 (type line K586). Mutants rms6-1 and rms6-2 were derived from dwarf and tall cultivars, Solara and Torsdag, respectively. The rms6 mutants are characterized by increased branching from basal nodes. In contrast, mutants rms1 through rms5 have increased branching from both basal and aerial (upper stem) nodes. Buds at the cotyledonary node of wild-type (WT) plants remain dormant but in rms6 plants these buds were usually released from dormancy. Their growth was either subsequently inhibited, sometimes even prior to emergence above ground, or they grew into secondary stems. The mutant phenotype was strongest for rms6-1 on the dwarf background. Although rms6-2 had a weak single-mutant phenotype, the rms3-1 rms6-2 double mutant showed clear transgression and an additive branching phenotype, with a total lateral length almost 2-fold greater than rms3-1 and nearly 5-fold greater than rms6-2. Grafting studies between WT and rms6-1 plants demonstrated the primary action of Rms6 may be confined to the shoot. Young WT and rms6-1 shoots had similar auxin levels, and decapitated plants had a similar magnitude of response to applied auxin. Abscisic acid levels were elevated 2-fold at node 2 of young rms6-1 plants. The Rms6 locus mapped to the R to Gp segment of linkage group V (chromosome 3). The rms6 mutants will be useful for basic research and also have possible agronomical value.

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