FINE CULM1 (FC1) Works Downstream of Strigolactones to Inhibit the Outgrowth of Axillary Buds in Rice

Abstract

Recent studies of highly branched mutants of pea, Arabidopsis and rice have demonstrated that strigolactones (SLs) act as hormones that inhibit shoot branching. The identification of genes that work downstream of SLs is required for a better understanding of how SLs control the growth of axillary buds. We found that the increased tillering phenotype of fine culm1 (fc1) mutants of rice is not rescued by the application of 1 μM GR24, a synthetic SL analog. Treatment with a high concentration of GR24 (10 μM) causes suppression of tiller growth in wild-type plants, but is not effective on fc1 mutants, implying that proper FC1 functioning is required for SLs to inhibit bud growth. Overexpression of FC1 partially rescued d3-2 defects in the tiller growth and plant height. An in situ hybridization analysis showed that FC1 mRNA accumulates in axillary buds, the shoot apical meristem, young leaves, vascular tissues and the tips of crown roots. FC1 mRNA expression was not significantly affected by GR24, suggesting that transcriptional induction may not be the mechanism by which SLs affect FC1 functioning. On the other hand, the expression level of FC1 is negatively regulated by cytokinin treatment. We propose that FC1 acts as an integrator of multiple signaling pathways and is essential to the fine-tuning of shoot branching in rice.

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

“…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). However, in rice, SL regulation of FC1 expression is not observed, and overexpression of FC1 in the d3 mutant only partially rescues the branching phenotype (Minakuchi et al, 2010). Action of SLs in rice may thus involve an alternate pathway that does not require function of the Tb1 ortholog, FC1, to inhibit outgrowth of branches (Minakuchi et al, 2010).…”

“…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).…”

“…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).…”

“…However, in rice, SL regulation of FC1 expression is not observed, and overexpression of FC1 in the d3 mutant only partially rescues the branching phenotype (Minakuchi et al, 2010). Action of SLs in rice may thus involve an alternate pathway that does not require function of the Tb1 ortholog, FC1, to inhibit outgrowth of branches (Minakuchi et al, 2010).…”