Mutants at the Slender1 Locus of Barley cv Himalaya. Molecular and Physiological Characterization

Abstract

A dominant dwarf mutant of barley (Hordeum vulgare) that resembles dominant gibberellin (GA) "-insensitive" or "-nonresponsive" mutants in other species is described. ␣-Amylase production by endosperm half-grains of the mutant required GA 3 at concentrations about 100 times that of the WT. The mutant showed only a slight growth response to GA 3 , even at very high concentrations. However, when additionally dwarfed, growth rate responded to GA 3 over the normal concentration range, although only back to the original (dwarf) elongation rate. Genetic studies indicated that the dominant dwarf locus was either closely linked or identical to the Sln1 (Slender1) locus. A barley sequence related to Arabidopsis GAI/RGA was isolated, and shown to represent the Sln1 locus by the analysis of sln1 mutants. The dominant dwarf mutant was also altered in this sequence, indicating that it too is an allele at Sln1. Thus, mutations at Sln1 generate plants of radically different phenotypes; either dwarfs that are largely dominant and GA "-insensitive/-nonresponsive," or the recessive slender types in which GA responses appear to be constitutive. Immunoblotting studies showed that in growing leaves, SLN1 protein localized almost exclusively to the leaf elongation zone. In mutants at the Sln1 locus, there were differences in both the abundance and distribution of SLN1 protein, and large changes in the amounts of bioactive GAs, and of their metabolic precursors and catabolites. These results suggest that there are dynamic interactions between SLN1 protein and GA content in determining leaf elongation rate.

Genetic Characterization and Functional Analysis of the GID1 Gibberellin Receptors inArabidopsis

“…By contrast, the DELLA domain is only present in the DELLA proteins and is essential for their degradation in response to GA, although it is not required for F-box protein binding. A number of DELLA gain-of-function mutations have been described; all except one are located in the DELLA regulatory domain (Peng et al, 1997(Peng et al, , 1999Boss and Thomas, 2002;Chandler et al, 2002;Muangprom et al, 2005). Deletions or specific missense mutations of the conserved motifs (DELLA and/or VHYNP) within the DELLA domain render the mutant proteins resistant to GA-induced degradation, leading to a GA-insensitive dwarf phenotype Gubler et al, 2002;Itoh et al, 2002).…”

“…The most extensively studied components of the GA signaling cascade are the DELLA proteins, which act as repressors of GAresponsive growth (Peng et al, 1997;Silverstone et al, 1998;Ikeda et al, 2001;Chandler et al, 2002). In the Arabidopsis genome, there are five DELLA genes , GA-INSENSITIVE [GAI], RGA-LIKE1 [RGL1], RGL2, and RGL3), whereas rice contains one, SLENDER RICE1 (SLR1; Itoh et al, 2002).…”

Common mechanisms regulating expression of rice aleurone genes that contribute to the primary response for gibberellin

“…Loss-of-function mutations in the DELLA gene produce a constitutive GA response phenotype in some cases [9,10]. Expression of the DELLA protein lacking the DELLA domain, which is a constitutive repressor form, shows a dominant GA-insensitive phenotype [9,10,11,12]. These results provide a reliable concept that the DELLA proteins are robust repressors of GA signaling and the functions of GA are established by removing the repressions of the DELLA proteins [6,13].…”

“…In contrast to Arabidopsis, GA response system of small cereal plants is simple. Each of rice and barley has a single DELLA gene, SLR1 and SLN1, so that recessive mutations of each gene exhibit solo deficiencies in the GA-regulated growth [9,10]. Upon application of GA, these DELLA proteins disappear in aleurone [8], young leaf [7] and anther [25], but visible physiological responses are differing in each tissue.…”

“…The DELLA proteins, a subgroup of the GRAS family of putative transcription factors [5], are located in the nucleus and rapidly disappeared after GA application [6,7,8]. Loss-of-function mutations in the DELLA gene produce a constitutive GA response phenotype in some cases [9,10]. Expression of the DELLA protein lacking the DELLA domain, which is a constitutive repressor form, shows a dominant GA-insensitive phenotype [9,10,11,12].…”