8th INTERNATIONAL WHEAT CONFERENCE

STRATegIeS foR ImPRoVINg WheAT ReSISTANCe
To NeCRoTRoPhIC dISeASeS
Robert Loughman 1 , Manisha Shankar 1 , Michael
Francki 1 , Robin Wilson 2 and Richard Oliver 3
1 Department of Agriculture and Food, Western Australia, 3 Baron-Hay Court, South Perth
6151 Australia; 2 InterGrain Pty Ltd, PO Box 4100 Victoria Park, 6100; 3 Curtin University
of Technology, GPO Box U1987 Perth, Western Australia 6845.
robert.loughman@agric.wa.gov.au
Foliar necrotrophic diseases such as tan spot (TS) caused by Pyrenophora tritici-repentis
(Died.) Drechs. and stagonospora nodorum blotch (SNB) caused by Phaeosphaeria nodorum
(E. Müller) Hedjaroude present resistance breeding targets in Australia as in many
other wheat growing regions. Stubble retention farming optimised with efficient chemical
weed control has favoured these leaf diseases which affect both yield and quality through
the production of shrivelled and poor coloured grain. The two pathogens are sufficiently
similar in their ecology to frequently occur together as a disease complex. Improving resistance
to necrotrophic diseases remains a challenging area in wheat breeding hampered
by both the quantitative control and partial expression of resistance. Phenotypic selection
is frequently laborious and significantly influenced by plant growth stage and environment.
Improving disease resistance is compromised by the need to achieve gains in other
breeding objectives.
Resistance to both pathogens is partial, generally expressed as restricted or slower lesion
development. There has been some success in sourcing SNB resistance for breeding
winter wheat germplasm. Resistance to SNB in white-grained spring wheats has been
more problematic due to grain softness, low flour yield and high α-amylase activity. For
TS, resistance expression in bread wheat sources has been less problematic. Surveillance
outside the adapted primary gene pools, including synthetic bread wheats and wheat
relatives, has also confirmed the reliance on partial resistance for both diseases. Effective
resistance sources in this context are a balance between the expression of resistance,
frequency in adapted gene pools, behaviour in breeding and association of penalties
through linkage drag.
Genetic studies have broadly focused on the inheritance of resistance in i) adapted germplasm,
ii) germplasm potentially contributing resistance effects through gene diversity
and iii) where genetic materials differentiate host response to specific fungal products as
qualitative responses corresponding to quantitative trait loci for disease response to the
pathogen. An international focus on these two necrotrophs has advanced a considerable
understanding of the underlying mechanism of disease determined by multiple proteinaceous
host-specific toxins (HSTs) that act in an inverse gene-for-gene manner. This international
research effort has characterised at least five S. nodorum HSTs as necrotrophic
effectors and three P. tritici-repentis effectors that interact with specific host sensitivity
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