A suppressor screen using the dwarf Rht-B1c Della mutant of wheat (Triticum aestivum L.) led to the isolation of overgrowth mutants, which retained the original dwarfing gene but grew at a faster rate because of a new mutation elsewhere in that gene. Forty-six alleles were identified, which included amino acid substitutions, premature stop codons, and splice site alterations. The sites of amino acid substitution were primarily localised around conserved motifs in the DELLA protein, and these mutants showed a wide range in their extent of growth recovery (dwarf, semidwarf, tall). Detailed growth comparisons were made on a wide height range of backcrossed overgrowth alleles, comparing stem and spike growth, leaf size, tillering, phenological development, coleoptile length, grain dormancy and grain yield. There were large and reproducible differences between alleles for some traits, whereas others were largely unaffected or varied with growth conditions. Some of the overgrowth alleles offer promise as alternatives to the Rht-B1b and Rht-D1b dwarfing genes, allowing a wider range of height control, improved grain dormancy and equivalent grain yield. The collection of mutants will also be valuable as a resource to study the effect of height on different physiological or agronomic traits, and in elucidating DELLA protein function.

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Many deletions of the wheat Della ( Rht - B1 ) gene and its flanking regions were isolated in a simple phenotypic screen, and characterised by modified analysis of SNP hybridisation data and cytogenetics. In a dwarf wheat suppressor screen, many tall 'revertants' were isolated following mutagenesis of a severely dwarfed (Rht-B1c) hexaploid wheat. About 150 lines were identified as putative deletions of Rht-B1c, based on the PCR analysis. Southern blot hybridisation established that most of them lacked the Rht-B1 gene, but retained the homoeologues Rht-A1 and Rht-D1. PCR assays were developed for orthologues of two genes that flank Rht-1/Della in the genomes of the model species Brachypodium and rice. Deletion of the B-genome-specific homoeologues of these two genes was confirmed in the Rht-B1 deletion lines, indicating loss of more than a single gene. SNP chip hybridisation analysis established the extents of deletion in these lines. Based on the synteny with Brachypodium chromosomes 1 and 4 g, and rice chromosomes 3g and 11g, notional deletion maps were established. The deletions ranged from interstitial deletions of 4BS through to loss of all 4BS markers. There were also instances, where all 4BS and 4BL markers were lost, and these lines had poor fertility and narrow stems and leaves. Cytogenetic studies on selected lines confirmed the loss of portions of 4BS in lines that lacked most or all 4BS markers. They also confirmed that lines lacking both 4BS and 4BL markers were nullisomics for 4B. These nested deletion lines share a common genetic background and will have applications in assigning markers to regions of 4BS as well as to 4BL. The potential for this type of analysis in other regions of the wheat genome is discussed.

In this chapter we discuss interactions between the gibberellins (GAs) and other plant hormones. Auxin and ethylene exert strong effects on GA levels, and at least some of the physiological responses to auxin are mediated by increased GA content. Abscisic acid (ABA) and GA appear to negatively regulate each other's levels in seeds, consistent with their antagonistic effects on germination. It has been suggested that several non‐GA hormones affect the stability of DELLAs, the key signalling proteins that are destabilised by GAs. However, it appears that the reported effects of these additional hormones on DELLA stability are either mediated by changes in GA content, or have not yet been confirmed. Recent papers provide evidence that DELLAs physically interact with transcriptional regulators from the signalling pathways of the brassinosteroids, ethylene, jasmonic acid and ABA. This may represent a physiologically significant way in which GAs interact with other signalling pathways, and helps to explain how DELLAs, which lack a conserved DNA binding domain, can regulate gene transcription.