A high-throughput phenotyping tool to identify field-relevant anthracnose resistance in white lupin

Summary

The seed- and air-borne pathogen Colletotrichum lupini, the causal agent of lupin anthracnose, is the most important disease in white lupin (Lupinus albus) worldwide and can cause total yield loss. The aims of this study were to establish a reliable high-throughput phenotyping tool to identify anthracnose resistance in white lupin germplasm and to evaluate a genomic prediction model, accounting previously reported resistance QTLs, on a set of independent lupin genotypes. Phenotyping under controlled conditions, performing stem inoculation on seedlings, showed to be applicable for high-throughput and its disease score strongly correlated with field plot disease assessments (r = 0.95, p<0.0001) and yield (r = -0.64, p=0.035). Traditional 1-row field disease phenotyping showed no significant correlation with field plot disease assessments (r = 0.31, p=0.34) and yield (r = -0.45, p=0.17). Genomically-predicted resistance values showed no correlation with values observed under controlled or field conditions, and the parental lines of the RIL population used for constructing the prediction model exhibited a resistance pattern opposite to that displayed in the original (Australian) environment used for model construction. Differing environmental conditions, inoculation procedures or population structure may account for this result. Phenotyping a diverse set of 40 white lupin accessions under controlled conditions revealed eight accessions with improved resistance to anthracnose. The standardized area under the disease progress curves (sAUDPC) ranged from 2.1 to 2.8 compared to the susceptible reference accession with a sAUDPC of 3.85. These accessions can be incorporated into white lupin breeding programs. In conclusion, our data supports stem inoculation-based disease phenotyping under controlled conditions as a time-effective approach to identify field-relevant resistance which can now be applied to further identify sources of resistance and their underlying genetics.