Display options
Share it on

Phytopathology. 1997 Jun;87(6):594-8. doi: 10.1094/PHYTO.1997.87.6.594.

Inheritance of Resistance to Leptosphaeria maculans in Brassica juncea.

Phytopathology

M Keri, C G van den Berg, P B McVetty, S R Rimmer

PMID: 18945075 DOI: 10.1094/PHYTO.1997.87.6.594

Abstract

ABSTRACT The inheritance of resistance to Leptosphaeria maculans, the causal agent of black leg of crucifers, was studied in Brassica juncea. Three resistant accessions (UM3021, UM3043, and UM3323) and one susceptible accession (UM3132) of B. juncea were crossed in a complete diallel. Parents, F(1), and F(2) progenies were evaluated for all crosses using both cotyledon and stem inoculation. Cotyledon reaction was evaluated with two isolates of L. maculans, but stem reaction was evaluated with one isolate. Disease reactions observed for individual plants were the same for both inoculation methods and for both isolates of the pathogen for cotyledon reaction. No segregation was observed for the crosses between resistant accessions (UM3043 x UM3323 and UM3021 x UM3323), but a few susceptible plants were observed in the F(2) progeny of crosses between resistant parents (UM3021 x UM3043). This was probably due to heterozygosity in some parental plants of UM3021. For crosses be tween the susceptible parent and resistant parents, F(1) plants for two crosses were all resistant. For cross UM3132 x UM3021, some susceptible plants occurred, which was also suggestive of heterozygosity in UM3021. Although resistance in F(1) was dominant, for F(2) populations, segregation fit either 13:3, 3:1, or 1:3 ratios, indicating that resistance can be either adominant or recessive trait. F(3) families derived from some susceptible F(2) plants from crosses UM3021 x UM3132 and UM3043 x UM3132 were evaluated using the cotyledon inoculation method only. Segregation of F(2) plants and F(3) families in crosses involving resistant and susceptible parents indicated that the resistance to L. maculans in B. juncea is controlled by two nuclear genes with dominant recessive epistatic gene action.

Publication Types