The identification of QTL controlling ergot sclerotia size in hexaploid wheat implicates a role for the Rht dwarfing alleles.
Four QTL conferring resistance to ergot were identified in the UK winter wheat varieties 'Robigus' and 'Solstice'. Two QTL co-located with semi-dwarfing alleles at the Rht loci Rht - 1B and Rht - 1D implicating a role of these DELLA proteins in infection success of Claviceps purpurea. The fungal pathogen Claviceps purpurea infects ovaries of a broad range of temperate grasses and cereals, including hexaploid wheat, causing a disease commonly known as ergot. Sclerotia produced in place of seed carry a cocktail of harmful alkaloid compounds that result in a range of symptoms in humans and animals, causing ergotism. Following a field assessment of C. purpurea infection in winter wheat, two varieties 'Robigus' and 'Solstice' were selected which consistently produced the largest differential effect on ergot sclerotia weights. They were crossed to produce a doubled haploid mapping population, and a marker map, consisting of 714 genetic loci and a total length of 2895 cM was produced. Four ergot reducing QTL were identified using both sclerotia weight and size as phenotypic parameters; QCp.niab.2A and QCp.niab.4B being detected in the wheat variety 'Robigus', and QCp.niab.6A and QCp.niab.4D in the variety 'Solstice'. The ergot resistance QTL QCp.niab.4B and QCp.niab.4D peaks mapped to the same markers as the known reduced height (Rht) loci on chromosomes 4B and 4D, Rht-B1 and Rht-D1, respectively. In both cases, the reduction in sclerotia weight and size was associated with the semi-dwarfing alleles, Rht-B1b from 'Robigus' and Rht-D1b from 'Solstice'. Two-dimensional, two-QTL scans identified significant additive interactions between QTL QCp.niab.4B and QCp.niab.4D, and between QCp.niab.2A and QCp.niab.4B when looking at sclerotia size, but not between QCp.niab.2A and QCp.niab.4D. The two plant height QTL, QPh.niab.4B and QPh.niab.4D, which mapped to the same locations as QCp.niab.4B and QCp.niab.4D, also displayed significant genetic interactions.
NIAB, Huntingdon Road, Cambridge, CB3 0LE, UK. anna.gordon@niab.com.
Anna
A
Gordon
NIAB, Huntingdon Road, Cambridge, CB3 0LE, UK.
Ryan
R
Basler
NIAB, Huntingdon Road, Cambridge, CB3 0LE, UK.|Syngenta France, Route de Moyencourt, 78910, Orgerus, France.
Pauline
P
Bansept-Basler
NIAB, Huntingdon Road, Cambridge, CB3 0LE, UK.
Vicky
V
Fanstone
NIAB, Huntingdon Road, Cambridge, CB3 0LE, UK.|Bayer CropScience, Department Technologiepark 38, 9052, Ghent, Belgium.
Lakshmi
L
Harinarayan
Department of Plant Sciences, University of Cambridge, Cambridge, CB2 3EA, UK.
Paul K
PK
Grant
NIAB, Huntingdon Road, Cambridge, CB3 0LE, UK.
Richard
R
Birchmore
NIAB, Huntingdon Road, Cambridge, CB3 0LE, UK.|Woodgate Farm, Cascob, Presteigne, Powys, LD8 2NT, UK.
Rosemary A
RA
Bayles
NIAB, Huntingdon Road, Cambridge, CB3 0LE, UK.
Lesley A
LA
Boyd
NIAB, Huntingdon Road, Cambridge, CB3 0LE, UK.|School of Agriculture, Policy and Development, University of Reading, Reading, RG6 6AR, UK.
Donal M
DM
O'Sullivan
D000483:Alleles; D001203:Ascomycota; D002874:Chromosome Mapping; D003433:Crosses, Genetic; D060467:Disease Resistance / Q000235:genetics*; D005838:Genotype; D006238:Haploidy; D010641:Phenotype; D010935:Plant Diseases / Q000235:genetics* / Q000382:microbiology; D040641:Quantitative Trait Loci; D014908:Triticum / Q000235:genetics* / Q000382:microbiology