Quantitative Inheritance of Sclerotinia Stem Rot Resistance in Brassica napus and Relationship to Cotyledon and Leaf Resistances

Abstract

Sclerotinia sclerotiorum is a necrotrophic fungus causing devastating stem rot and associated yield losses of canola/rapeseed (Brassica napus) worldwide, including in Australia. Developing host resistance against Sclerotinia stem rot is critical if this disease in canola/rapeseed is to be successfully managed, as cultural or chemical control options provide only partial or sporadic control. Three B. napus breeding populations, C2, C5 and C6, including the parents, F1, F2, BC1P1 and BC2P2, were utilised in a field study with an objective of exploring the inheritance pattern of disease resistance (based on stem lesion length, SLL), the genetic relationships of disease with stem diameter (SD) or days to flowering (DTF), and to compare these new adult plant stem resistances against S. sclerotiorum with those of seedling (cotyledon and leaf) resistances in earlier studies. Heritability (broad-sense) of SLL, was 0.57 and 0.73 for populations C2 at 3 and 5 weeks post-inoculation, and was 0.21 for C5 at 5 weeks post-inoculation. Additive genetic variance was evident within all three populations for DTF but not for SD. Narrow sense heritability for DTF was 0.48 (C2), 0.42 (C5) and 0.32 (C6). SD, DTF and SLL were all inherited independently with no significant genetic covariance between traits in bivariate analysis. Genetic variance for SLL in populations C2 and C5 was entirely non-additive, and there was significant non-additive genetic covariance of SLL at 3 and 5 weeks post-inoculation. Generation means analysis in population C2 supported the conclusion that complex epistatic interactions controlled SLL. Several C2 and C5 progeny showed high adult plant stem resistance which may be critical in developing enhanced stem resistance in canola/rapeseed. While population C6 showed no genetic variation for SLL resistance in this study, it showed significant non-additive genetic variance at the cotyledon and leaf stages in earlier studies. We conclude that host resistance varies across different plant growth stages and breeding must be targeted for resistance at each growth stage. In populations C2, C5 and C6, resistance to S. sclerotiorum in stem, leaf and cotyledon is always controlled by non-additive effects such as complex epistasis or dominance. Overall, our findings in relation to the quantitative inheritance of Sclerotinia stem rot resistance, together with the new, high-level resistances identified, will enable breeders to select/develop genotypes with enhanced resistances to S. sclerotiorum.

Genetic Analysis for Resistance to Sclerotinia Stem Rot, Yield and Its Component Traits in Indian Mustard [Brassica juncea (L.) Czern & Coss.]

“…Both additive and non-additive genetic effects influenced Sclerotinia stem rot resistance, as evidenced by significant mean squares of lines, testers, and line × tester interactions for both resistance evaluation criteria, namely, MLL and DSI. These findings are consistent with those of Khan et al [ 32 ], Disi et al [ 30 ], Godoy et al [ 59 ], Castano et al [ 60 ], and Achbani et al [ 61 ], who found that both additive and non-additive genetic action influenced Sclerotinia rot resistance inheritance and could be improved using the recurrent selection procedure. The significant effect of GCA on the sum of squares of SCA suggested that early generation selection of resistant progenies could be successful.…”

“…The heritability of Sclerotinia stem rot resistance evaluation parameters (MLL and DSI) was moderate, indicating that early selection for Sclerotinia stem rot resistance may be successful. Sclerotinia stem rot resistance has been estimated to be heritable by various researchers, with values ranging from 21 to 88% [ 32 , 84 , 85 ]. Genetic advance as percent of mean (GAM) values are divided into three categories: low (0–10%), moderate (10–20%), and high (>20%) [ 86 ].…”

“…However, a lack of suitable resistant sources has hampered breeding for resistance in the past. Previous attempts to uncover resistant sources against Sclerotinia stem rot failed miserably because all Indian mustard genotypes tested were sensitive/highly susceptible, and whatever resistant sources were declared were connected to wild and other Brassicaceae species [ 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 ]. However, in recent years, increased attention has led to identifying a few Indian mustard genotypes resistant to the disease [ 1 , 6 , 33 , 34 , 35 ].…”

Genetic and Proteomic Basis of Sclerotinia Stem Rot Resistance in Indian Mustard [Brassica juncea (L.) Czern & Coss.]

“…Information regarding the pattern of inheritance as well as the nature of gene action involved in resistance against Sclerotinia sclerotiorum helps crop geneticists and breeders to elect appropriate selection methods for breeding resistant cultivars. Previous studies have revealed that inheritance of Sclerotinia stem rot resistance varies from crop to crop being monogenic in Vicia faba [55] while polygenic in B. napus [23,32]. Our study is perhaps the first to report on the genetic investigation and protein expression patterns of Sclerotinia stem rot resistance in B. juncea.…”

“…Therefore, host genetic resistance is the most convenient, economic, and eco-friendly approach for the effective control of this devastating pathogen [18,19]. Earlier attempts to identify resistant sources against this disease in Indian mustard were hampered as all the B. juncea genotypes evaluated were found susceptible to Sclerotinia stem rot and any of the resistant sources reported belonged to other cruciferous crops and its wild relatives such as Brassica napus, B. fruticulosa, B. rupestris, B. incana, B. insularis, B. villosa, Erucastrum cardaminoides, E. abyssinicum, Sinapis alba, and Diplotaxis tenuisiliqua [20][21][22][23][24][25][26][27][28][29][30][31][32], with no reports available about its resistance in B. juncea, which is an important oil yielding crop in the Indian context. However, in recent few years, increasing attention has been paid which has ultimately led to the identification of a few Indian mustard genotypes resistant against this pathogen [3,5,33,34].…”