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Sclerotinia rot, caused by the fungal pathogen Sclerotinia sclerotiorum, is a devastating disease on oilseed rape and mustard worldwide. While the focus to effectively control yield losses from Sclerotinia has been on locating stem resistance, resistance to leaf and to early (cotyledon) stage resistance to this pathogen are also important, both not only limiting additional plant damage, but also inoculum build up and spread onto stems. Three Brassica napus breeding populations developed in India, C2 (NC-8 × RQ-001-NCA-8 NC2-7), C5 (cv. Charlton × RQ-001-NCA-8 NC2-7) and C6 (cv. Charlton × NC4-5), were screened for cotyledon resistance (based on lesion diameter) under controlled environmental conditions to investigate the inheritance of disease resistance. Each population consisted of parents (P1 and P2), F1, F2, BC1P1 and BC2P2, except for population C5 which lacked BC1P1. Moderate broad sense heritability of 0.42, 0.31 and 0.49 for cotyledon resistance was found in populations C2, C5 and C6, respectively, and there was mostly non-additive genetic control of resistance. Analyses of generation means and variances indicated that the additive-dominance model was adequate to explain genetics of cotyledon resistance in population C2. There was heterosis for susceptibility (i.e., larger lesion diameter). The dominance × dominance digenic epistasis explained genetic control in population C6, with heterosis towards resistance (i.e., smaller lesion diameter). This information is critical for breeding for resistance to this important pathogen in Australia, India and elsewhere. [ABSTRACT FROM AUTHOR]