Characterizing Chromosomes for Fusarium Head Blight Resistance in a Spring Wheat (Triticum aestivum L.) Cultivar, 'Frontana'
Abstract
Fusarium head blight (FHB), caused by the fungus Fusarium graminearum, is a major
fungal disease of wheat and other cereal crops that causes both yield and quality losses due
to shriveled kernels and accumulation of mycotoxins in the seed. 'Frontana', a Brazilian
spring wheat cultivar, is a source ofresistance genes to FHB, and it is believed to express
resistance to both the establishment and spread of FHB (type I and type II resistance,
respectively). Reciprocal backcross monosomic (RBCM) lines developed using Frontana
and 'Chris', a susceptible spring wheat cultivar, and involving critical chromosomes 3A,
6A, and 4D from these parents were compared to characterize the type of resistance
expressed by Frontana and confirm the chromosomes carrying genes for resistance. In
four separate greenhouse tests, spray and single floret inoculation techniques were used to
assess both types of resistance. Plants were inoculated when half of the plants in a pot were
at anthesis (Feekes Growth Stage 10.5). Genotypes were evaluated for disease incidence,
spread, deoxynivalinol (DON) content, Fusarium damaged kernels (FDK) and severity at
21 d after inoculation. Generally, RBCM lines with the critical Frontana chromosomes had
low FHB incidence, spread, and severity. The RBCM line with chromosome 3A from
Frontana exhibited the lowest FHB severity after spray inoculation, and the least spread
after point inoculation. Frontana 3A lines had the lowest FHB incidence levels after spray
inoculation amongst the RBCM lines that were tested. This implies the presence of major resistance genes on chromosome 3A which are likely involved in both resistance to disease
establishment and spread. However, resistance genes on 3A likely also interact with genes
on other chromosomes to confer resistance to FHB because Frontana typically expressed a
higher level of resistance to disease establishment and spread. Chromosome 4D also seems
to play a significant role in Type I resistance while 6A contributes to Type II resistance.