The Pea TCP Transcription Factor PsBRC1 Acts Downstream of Strigolactones to Control Shoot Branching  

Abstract

The function of PsBRC1, the pea (Pisum sativum) homolog of the maize (Zea mays) TEOSINTE BRANCHED1 and the Arabidopsis (Arabidopsis thaliana) BRANCHED1 (AtBRC1) genes, was investigated. The pea Psbrc1 mutant displays an increased shoot-branching phenotype, is able to synthesize strigolactone (SL), and does not respond to SL application. The level of pleiotropy of the SL-deficient ramosus1 (rms1) mutant is higher than in the Psbrc1 mutant, rms1 exhibiting a relatively dwarf phenotype and more extensive branching at upper nodes. The PsBRC1 gene is mostly expressed in the axillary bud and is transcriptionally up-regulated by direct application of the synthetic SL GR24 and down-regulated by the cytokinin (CK) 6-benzylaminopurine. The results suggest that PsBRC1 may have a role in integrating SL and CK signals and that SLs act directly within the bud to regulate its outgrowth. However, the Psbrc1 mutant responds to 6-benzylaminopurine application and decapitation by increasing axillary bud length, implicating a PsBRC1-independent component of the CK response in sustained bud growth. In contrast to other SL-related mutants, the Psbrc1 mutation does not cause a decrease in the CK zeatin riboside in the xylem sap or a strong increase in RMS1 transcript levels, suggesting that the RMS2-dependent feedback is not activated in this mutant. Surprisingly, the double rms1 Psbrc1 mutant displays a strong increase in numbers of branches at cotyledonary nodes, whereas branching at upper nodes is not significantly higher than the branching in rms1. This phenotype indicates a localized regulation of branching at these nodes specific to pea.

SMAX1-LIKE7 signals from the nucleus to regulate shoot development in Arabidopsis via partially EAR motif-independent mechanisms

“…The role of SLs in regulating shoot branching has been intensively studied, resulting in two contrasting, nonexclusive models for their mode of action. In the first, SLs are proposed to act locally in axillary buds by upregulating the expression of the BRANCHED1 (BRC1) gene, which encodes a TEOSINTE BRANCHED1/CYCLOIDEA/PCNA domain transcription factor (Braun et al, 2012). BRC1 is well-established as a regulator of bud outgrowth, and brc1 mutants have strongly increased, SL-resistant branching (Aguilar-Martínez et al, 2007;Brewer et al, 2009).…”

Diverse Roles of Strigolactone Signaling in Maize Architecture and the Uncoupling of a Branching-Specific Subnetwork

“…Placement of Tb1 orthologs downstream of SL signaling is based on two observations. First, brc and fc1 mutants do not respond to SL treatment (Brewer et al, 2009;Minakuchi et al, 2010;Braun et al, 2012). Second, double mutant combinations constructed in diverse species, including Atbrc1 max3, Atbrc1 max4, Psbrc1 rms1, and fc1 d17 (Aguilar-Martínez et al, 2007;Minakuchi et al, 2010;Braun et al, 2012), consistently show branching phenotypes that resemble the corresponding SL-deficient single mutant.…”

“…First, brc and fc1 mutants do not respond to SL treatment (Brewer et al, 2009;Minakuchi et al, 2010;Braun et al, 2012). Second, double mutant combinations constructed in diverse species, including Atbrc1 max3, Atbrc1 max4, Psbrc1 rms1, and fc1 d17 (Aguilar-Martínez et al, 2007;Minakuchi et al, 2010;Braun et al, 2012), consistently show branching phenotypes that resemble the corresponding SL-deficient single mutant. Additional support for this hypothesis is also available from Arabidopsis and pea, where expression of AtBRC1 and PsBRC1 is reduced in SL mutants (Aguilar-Martínez et al, 2007;Finlayson, 2007;Braun et al, 2012) and PsBRC1 expression is enhanced by SL treatment (Braun et al, 2012).…”

“…Genetic studies in Arabidopsis, pea, and rice implicate orthologs of the maize Teosinte Branched1 (Tb1) transcription factor (Doebley et al, 1997) as a key downstream target of SL signaling. In all three species, mutants of Tb1 orthologs, Atbrc1 (for branched1) and Atbrc2 of Arabidopsis (Aguilar-Martínez et al, 2007;Finlayson, 2007), Psbrc1 of pea (Braun et al, 2012), and fine culm1 (fc1) of rice (Minakuchi et al, 2010), cause increased branching phenotypes. In Arabidopsis, AtBRC1 and AtBRC2 function as integrators for phytochrome regulation of branching (Finlayson et al, 2010).…”

Using Arabidopsis to Study Shoot Branching in Biomass Willow

“…This could be achieved by influencing the transcription of growth-regulating genes in the bud (Aguilar-Martínez et al, 2007;Brewer et al, 2009;Braun et al, 2012;Dun et al, 2012) and/or by modulating auxin transport properties, both locally and systemically, thereby affecting the ability of buds to establish auxin transport canalization into the main stem (Bennett et al, 2006;Lazar and Goodman, 2006;Lin et al, 2009;Prusinkiewicz et al, 2009;Crawford et al, 2010;Marhavý et al, 2011;Shinohara et al, 2013). Activation of buds will in turn affect the amount of auxin transported out into the main stem.…”