How do fungi interact with the Gibberellic acid pathways in developing wheat ovules and what are the implications for resistance and yield

Theme: Agriculture and Food Security

Two mycotoxin-producing wheat diseases have serious consequences for food safety in the UK and have GA implicated in their disease progression. This project involves a variety of techniques including microscopy, metabolite extraction and plant pathology and all with the UK's most valuable crop species - wheat.

Infection of grain by fungal pathogens results in yield loss and toxin contamination in cereal crops worldwide. Two important diseases of UK cereal production are caused by fungi with contrasting modes of ear/grain infection. The fungus Claviceps purpurea (Cp) infects wheat ovules, replacing the seed with fungal sclerotia and causing Ergot. Ergot sclerotia are full of a toxic alkaloids that in humans caused the medieval disease St Antony's Fire. The more opportunistic Fusarium pathogen complex (causing Fusarium Head Blight; FHB) infects all parts of the wheat ear, leading to production of harmful mycotoxins within the developing grain.

Ground-breaking research at NIAB indicates that Cp co-opts the plant's Gibberellic Acid (GA) pathways to establish infection and reproduce. Partial resistance to Ergot has been found to co-locate with the wheat dwarfing genes, Rht-1Bb and Rht-1Db (Gordon et al 2015; TAG in press). These DELLA protein mutants are non-responsive to GA, resulting in growth retardation (Peng et al 1999; Nature 40: 256). Preliminary results in wheat transgenic lines expressing a bean GA2 oxidase1 specifically in ovules indicates that lowering GA levels results in reduced Cp infection and smaller sclerotia. Resistance to FHB, which can be classified by infection type, has also been shown to be linked to the wheat dwarfing genes (Srinivasachary et al 2009; TAG 118: 695), GA being hypothesised to play a role in the ability of the fungus to spread within the ear.

An international collaboration with Canadian partners has yielded new resources including a hexaploid synthetic line containing very good ergot resistance (Menzies et al 2002) and a mapping population in order to map the genes responsible. We have mixed wheat-fungal transcriptome data from that population that is helping to identify fungal elicitors targets and further markers.

Outline:
- Full GA metabolic analysis to determine levels of GA during Cp and FHB disease progression in transgenic and wildtype lines.
- Transcriptome and GA analysis of Claviceps and Fusarium species' ability to co-opt host GA pathways or produce their own.
- An opportunity to breed real ergot resistance into UK wheat lines.