Roles for auxin, cytokinin, and strigolactone in regulating shoot branching

Ferguson, B. J. and Beveridge, C. A. (2009) Roles for auxin, cytokinin, and strigolactone in regulating shoot branching. Plant Physiology, 149 4: 1929-1944. doi:10.1104/pp.109.135475

Author Ferguson, B. J.
Beveridge, C. A.
Title Roles for auxin, cytokinin, and strigolactone in regulating shoot branching
Journal name Plant Physiology   Check publisher's open access policy
ISSN 0032-0889
Publication date 2009-04
Year available 2009
Sub-type Article (original research)
DOI 10.1104/pp.109.135475
Volume 149
Issue 4
Start page 1929
End page 1944
Total pages 16
Editor D. Ort
Place of publication United States
Publisher American Society of Plant Biologists
Collection year 2010
Language eng
Subject C1
829999 Plant Production and Plant Primary Products not elsewhere classified
060705 Plant Physiology
Formatted 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.
Keyword Phaseolus vulgaris L
Pisum sativum L
Cicer arietinum seedlings
Axillary bud outgrowth
Apical dominance
Pea seedlings
Indole-3-acetic acid levels
Correlative inhibition
1-Naphthylacetic acid
Nodule organogenesis
Q-Index Code C1
Q-Index Status Confirmed Code

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Created: Thu, 03 Sep 2009, 08:23:29 EST by Mr Andrew Martlew on behalf of Centre for Integrative Legume Research