Abstract
Many processes have been described in the control of shoot branching. Apical dominance is defined as the control exerted by the shoot tip on the outgrowth of axillary buds, whereas correlative inhibition includes the suppression of growth by other growing buds or shoots. The level, signaling, and/or flow of the plant hormone auxin in stems and buds is thought to be involved in these processes. In addition, RAMOSUS (RMS) branching genes in pea (Pisum sativum) control the synthesis and perception of a long-distance inhibitory branching signal produced in the stem and roots, a strigolactone or product. Auxin treatment affects the expression of RMS genes, but it is unclear whether the RMS network can regulate branching independently of auxin. Here, we explore whether apical dominance and correlative inhibition show independent or additive effects in rms mutant plants. Bud outgrowth and branch lengths are enhanced in decapitated and stem-girdled rms mutants compared with intact control plants. This may relate to an RMS-independent induction of axillary bud outgrowth by these treatments. Correlative inhibition was also apparent in rms mutant plants, again indicating an RMS-independent component. Treatments giving reductions in RMS1 and RMS5 gene expression, auxin transport, and auxin level in the main stem were not always sufficient to promote bud outgrowth. We suggest that this may relate to a failure to induce the expression of cytokinin biosynthesis genes, which always correlated with bud outgrowth in our treatments. We present a new model that accounts for apical dominance, correlative inhibition, RMS gene action, and auxin and cytokinin and their interactions in controlling the progression of buds through different control points from dormancy to sustained growth.
Highlights
Many processes have been described in the control of shoot branching
Homologous pathways have been identified in pea, Arabidopsis (Arabidopsis thaliana), and petunia (Petunia hybrida) and are regulated by RMS, MORE AXILLARY GROWTH (MAX), and DECREASED APICAL DOMINANCE (DAD) genes, respectively
We present findings from experiments in which we evaluated the effects of stem girdling, decapitation, and bud removal on branching in rms mutants to determine whether apical dominance, correlative inhibition, and the RMS/strigolactone pathway are independent or interconnected mechanisms
Summary
Morris et al (2005) used tall pea plants to demonstrate that IAA, at concentrations as high as 3 mg g21 in lanolin, diminished the amount of bud outgrowth following decapitation but was unable to completely prevent outgrowth from occurring. The trend observed was similar to that using decapitated plants (Fig. 4), suggesting that IAA has a similar role in decapitation- and stem girdling-induced bud outgrowth These findings are Defoliation is known to deplete stem auxin levels in pea (Jager et al, 2007). We explored whether a reduced supply of leaf-derived energy and/or signals could prevent the growth of buds induced to grow out This was tested by defoliating plants whose buds were triggered to grow by stem-girdling or decapitation treatments at upper nodes. These findings demonstrate that the complete lack of bud outgrowth ob-
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