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ARS Home » Midwest Area » St. Paul, Minnesota » Plant Science Research » Research » Publications at this Location » Publication #155753
Title: GENETIC CHARACTERIZATION OF FHB RESISTANCE SUPPRESSION CONDITIONED BY CHROMOSOME 2A OF TRITICUM DICOCCOIDES

Author
item STACK, R - NORTH DAKOTA STATE UNIV
item Garvin, David
item HANSEN, J - NORTH DAKOTA STATE UNIV

Submitted to: National Fusarium Head Blight Forum
Publication Type: Abstract Only
Publication Acceptance Date: 12/13/2003
Publication Date: 12/13/2003
Citation: Stack, R.W., Garvin, D.F., Hansen, J.M. 2003. Genetic characterization of FHB resistance suppression conditioned by chromosome 2A of Triticum dicoccoides [abstract]. National Fusarium Head Blight Forum Proceedings. p. 231.

Interpretive Summary:

Technical Abstract: Disomic substitution lines, LDN(DIC), prepared by replacing chromosomes of Langdon durum with those from T. dicoccoides (TDIC), showed highly significant differences in response to Fusarium head blight (FHB) when challenge inoculated with Fusarium graminearum in the greenhouse (Stack et al. 2002 Crop Science 42:637-642). Several of the LND(DIC) lines showed increased resistance to FHB. One line, LDN(DIC2A), was highly susceptible to FHB, just as is the TDIC accession that contributed the chromosomes to the substitution lines. In F1 hybrids with other substitution lines the gene(s) on 2A behaves as a "susceptibility gene" that acts in an additive manner. In most F1 hybrids involving LDN(DIC-2A), the FHB score was intermediate between the parents. In populations derived from crosses of the LDN(DIC-2A) to an FHB resistant line, such as LDN(DIC-3A), the FHB resistance frequency distribution in the F2 suggests that the gene(s) on chromosome 2A is epistatic to any resistance genes. The distribution of FHB severity values in the F2 exhibited a trimodal distribution suggestive of a 1:2:1 segregation ratio that may be expected due to segregation of a single gene that acts additively. This supports the hypothesis that a single gene is present on chromosome 2A that not only increases FHB susceptibility, but also suppresses the action of the chromosome 3A FHB resistance.