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Dosage Dependent Genetic Suppression of Oat Crown Rust Resistance Gene Pc-62

Dep. of Plant Sciences, 370D Loftsfard Hall, North Dakota State Univ., Fargo, ND 58105

^* Corresponding author (mmcmulle{at}plains.NoDak.edu).

Combining crown rust resistance (CRR) genes is an objective many oat (Avena sativa L.) breeding programs. Genetic suppressors of CRR have been reported, but the genetic nature of such suppressors has not been investigated. An excess of susceptible seedlings in segregating progeny of crosses involving genotypes with Pc-38 and Pc-62 suggested the Pc-38 parent may have a factor that inhibits the expression of Pc-62. Our objectives were to (i) examine a putative genetic interaction between oat CRR gene Pc-62 and a dominant suppressor, (ii) utilize chromosomine terchanges tocks to define genetically the location of the suppressor, (iii) evaluate the effect of gene dosage combinations on the resistance-suppression relationship, and (iv) examine alternative explanations of distorted segregation (genetic background and differential gametet ransmission). The use of duplication-deficiency (Dp-Df) genotypes placed a putative suppressor an interchanged chromosome segment that contains Pc-38. Resistance conferred by Pc-62 was suppressed in F₁ trisomic CRR locus combinations (1 Pc-62:2 Pc-38) in comparison to the expression of resistance in F₁ seedlings hemizygous for Pc-62. The Pc-38 segment contributed by two independently derived cultivars produced equivalent suppression in F₁ combinations with Pc-62. The presence of Pc-38 in an interchanged position in the cultivar Dumont allowed production of mono- and diallelic combinations of resistance genes and evaluation of mono-, di-, and trisomic segregation of the CRR locus. Diallelic trisomic segregation for the CRR locus indicated that an increasing dosage of Pc-62, relative to the suppressor and Pc-38, decreased the degree of suppression. Male transmission of Dp-Df gametes was not reduced relative to the frequency of gametes with a complete chromosome complement.

Received for publication February 21, 1996.