Analysis of the barley bract suppression gene Trd1

Abstract

A typical barley (Hordeum vulgare) floret consists of reproductive organs three stamens and a pistil, and non-reproductive organs-lodicules and two floral bracts, abaxial called 'lemma' and adaxial 'palea'. The floret is subtended by two additional bracts called outer or empty glumes. Together these organs form the basic structural unit of the grass inflorescence, a spikelet. There are commonly three spikelets at each rachis (floral stem of the barley spike) node, one central and two lateral spikelets. Rare naturally occurring or induced phenotypic variants that contain a third bract subtending the central spikelets have been described in barley. The gene responsible for this phenotype was called the THIRD OUTER GLUME1 (Trd1). The Trd1 mutants fail to suppress bract growth and as a result produce leaf-like structures that subtend each rachis node in the basal portion of the spike. Also, floral development at the collar is not always suppressed. In rice and maize, recessive mutations in NECK LEAF1 (Nl1) and TASSEL SHEATH1 (Tsh1) genes, respectively, have been shown to be responsible for orthologous phenotypes. Fine mapping of the trd1 phenotype in an F(3) recombinant population enabled us to position Trd1 on the long arm of chromosome 1H to a 10 cM region. We anchored this to a conserved syntenic region on rice chromosome Os05 and selected a set of candidate genes for validation by resequencing PCR amplicons from a series of independent mutant alleles. This analysis revealed that a GATA transcription factor, recently proposed to be Trd1, contained mutations in 10 out of 14 independent trd1 mutant alleles that would generate non-functional TRD1 proteins. Together with genetic linkage data, we confirm the identity of Trd1 as the GATA transcription factor ortholog of rice Nl1 and maize Tsh1 genes.

Induced Variations in Brassinosteroid Genes Define Barley Height and Sturdiness, and Expand the Green Revolution Genetic Toolkit

“…In the first case, the mutants were induced by identical chemical treatment (brh3.g, brh3.h, and brh3.i), in the second case by different treatments (ari-o.40, ari-o.43, and ari-o.143). In each case, the mutants were induced in the same mutagenesis program, and thus we cannot exclude a mix-up of mutant accessions after the mutagenic treatment as it was suggested earlier for alleles of barley loci praematurum-a and third outer glume1 (Houston et al, 2012;Zakhrabekova et al, 2012). Two other cases, however, strongly point toward an independent ancestry of identical mutations.…”

Variation in the interaction between alleles of HvAPETALA2 and microRNA172 determines the density of grains on the barley inflorescence

“…MLOC_81350 and MLOC_43830 were sequenced in the lines detailed in Dataset S1 exactly as described in Houston et al (8). Sequences were aligned using Geneious version 6.1.2 (Biomatters).…”

“…Spikes were harvested from WT and Zeo1.b plants at 12,18,22,26,31, and 36 dpg. Tissue was fixed and processed for scanning electron microscopy as described previously (8).…”

“…[2][3][4][5]. However, within the Triticeae cereals, a group that includes some of the world's most important human foods, only Q, a highly pleiotropic gene that influences a broad range of phenotypic characters including inflorescence compactness, fragility, and free-threshing (6), and genes that determine the development of an extra floret on the lemma (7), additional glumes (8), the number of grains on the inflorescence (9), and floret fertility (10) have been molecularly characterized.…”

A homolog of Blade-On-Petiole 1 and 2 (BOP1/2) controls internode length and homeotic changes of the barley inflorescence

“…The genes controlling barley inflorescence architecture and development have only been revealed for a few characters. Major genes that control row type (vrs1 [Komatsuda et al, 2007], intermedium-c [Ramsay et al, 2011], and vrs4 [Koppolu et al, 2013]), the conversion of awns into an extra floret (Hooded; Müller et al, 1995), adherence of the hull to the caryopsis (nud; Taketa et al, 2008), swelling of lodicules conferring open/ closed flowering (cleistogamy/chasmogamy) and spike density (cly1 [Nair et al, 2010] and zeo1 [Houston et al, 2013]), elongation of awns and pistil morphology (lks2; Yuo et al, 2012), suppression of bracts (trd1; Whipple et al, 2010;Houston et al, 2012), spike branching (com2; Poursarebani et al, 2015), and brittleness of the rachis (btr1/btr2; Pourkheirandish et al, 2015) were recently cloned. A large number of additional morphological mutants that influence barley inflorescence development (Forster et al, 2007) also have been described, and the underlying genes need to be identified to reach a more complete understanding of the regulatory pathways controlling barley spike architecture and development (Forster et al, 2007).…”