Submitted to: International Fusarium Workshop
Publication Type: Abstract only
Publication Acceptance Date: 12/11/2004
Publication Date: 12/11/2004
Citation: Garvin, D.F., Stack, R.W. 2004. Molecular genetics of Fusarium head blight susceptibility associated with chromosome 2a from the wild emmer line Israel A [abstract]. Proceedings of the 2nd International Symposium on Fusarium Head Blight. p. 60. Interpretive Summary:
Technical Abstract: The LDN(DIC) set of disomic substitution lines, in which chomosomes of durum wheat cv. Langdon (LDN) are replaced by corresponding ones from the wild emmer line 'Israel A' (DIC), have been useful in locating genes for resistance to Fusarium head blight (FHB). The line LDN(DIC-2A) shows increased FHB susceptibility relative to Langdon, suggesting the presence of a susceptibility factor on chromosome 2A from Israel A. We are interested in understanding the underlying biology associated with this increased FHB susceptibility. In previous studies we obtained evidence that this chromosome not only increases susceptibility but also appears to suppress the action of a major FHB resistance QTL locatd on chromosome 3A from Israel A. The gene or genes involved appear to act in an additive fashion. We are now seeking to further dissect the genetics of the FHB susceptibility through molecular mapping. A population of recombinant inbred lines (RICL) from the cross LDN(DIC-2A) x LDN was screened for FHB resistance. DNA from the parents was isolated and screened with microsatellite markers for chromosome 2A to identify polymorphisms that could be used for construction of a molecular map of this chromosome. The FHB disease index of the RICL ranged from 18 to 95, with a mean of 61. The disease index for LDN and LDN(DIC-2A) were approximately 45 and 80, respectively. Molecular markers spanning more than 100 cM of chromosome 2A were scored in the RICLs. QTL analysis revealed at least one region of chromosome 2A that was associated with increased susceptibility to FHB. Disease index means for individuals with alternate alleles at the microsatellite marker most strongly associated with FHB susceptibility differed by nearly 17% (71% vs 54%). We are adding additional molecular markers to the chromosome 2A map and are obtaining more FHB resistance data on the RICL population to be able to describe in more detail the molecular genetics of FHB susceptibility associated with this chromosome.