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SESSION 4: GENETICS OF HOSTS – PLANT RESISTANCE TO FUSARIUM,
VARIETY DEVELOPMENT
Semi-dwarf ‘uzu’ barley carries enhanced resistance
to a range of pathogens including Fusarium
culmorum
F. Doohan, L. Gunupuru, S. Ali
E-mail: fiona.doohan@ucd.ie
Brassinosteroids (BRs) are hormones that influence plant growth, development
and defence responses. The BR receptor protein Brassinosteroid Insensitive 1
(BRI1) has been characterised in several plant species. Semi-dwarf barley ‘uzu’
varieties have a mutation in the kinase domain of Bri1. In studies conducted using
barley genotypes Akashinriki and Bowman and their ‘uzu’ derivatives, we show
‘uzu’ is more resistant to Fusarium head blight (FHB) disease. Resistance was
characterised as the uzu plants having > 38% lower disease symptoms and >
25% higher yield as compared to parent lines Akashinriki and Bowman. Seedling
experiments showed that the ‘uzu’ derivative of Akashinriki was also 87% more
resistant to Fusarium seedling blight as compared to the parent line. Virusinduced
gene silencing of Bri1 lead to enhanced susceptibility of detached leaves
to Fusarium culmorum (>2 times more disease than plants treated with the empty
VIGS vector). Thus the Fusarium resistance of ‘uzu’ is not a consequence of
reduced BRI1 activity. Microarray analysis identified genes differentially regulated
between the mutant and wild type during disease development. We are currently
determining the effect of the uzu mutation on downstream BR signalling and the
functionality of the kinase domain of the uzu Bri1. Furthermore, studies on net
blotch disease and Barley Stripe Mosaic Virus show that ‘uzu’ confers broadspectrum
resistance. We now begin a four-year project in order to determine the
factors underpinning the ‘uzu’ associated resistance. We want to determine why
‘uzu’ has enhanced resistance to Fusarium and if any of the genes identified via
microarray of ‘uzu’/Akashinriki contribute to the Fusarium resistance inherent in
‘uzu’? Preliminary results show that the gene silencing of a membrane receptor
up-regulated in ‘uzu’ versus Akashinriki in response to Fusarium results in
enhanced Fusarium disease in detached leaf assays. Our second objective is to
determine if genes identified in other studies as contributing to Fusarium
resistance play a role in brassinosteroid signaling.
Acknowledgements: Dr. Sato, Barley Germplasm Centre, Kurashiki, Japan for
providing the Uzu and Akashinriki cultivar lines. Dr.Paul nicholson, JIC, Norwich
for providing Bowman and Bowman-Uzu cultivar lines. This work has emanated
from research conducted with the financial support of the Irish Department of
Agriculture, Food and the Marine and Science Foundation Ireland.
Keywords: Brassinosteroid, Fusarium, resistance
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