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Management of plant disease in agro-ecosystems ideally relies on a combination of host genetic resistance, chemical control, and cultural practices. Growers increasingly rely on chemical and genetic options, but their relative benefits in disease control, yield, and economic outcomes are rarely quantified. We explore this relationship for blackleg crown canker disease (caused by Leptosphaeria maculans ), a major biotic constraint limiting canola production globally. Data from 20 field trials conducted from 2013 to 2015 in canola-growing regions of Australia were used to assess the effects of host resistance and fungicide treatment on blackleg severity, grain yield, and gross margin. In the absence of fungicide, blackleg disease was 88% lower in the most resistant compared with the most susceptible blackleg resistance category. In the most susceptible resistance category, the most effective fungicide treatment significantly reduced blackleg severity (from 50 to 6%) and increased grain yield (478 kg/ha, 41%) and gross margin (AU$120/ha, 17%). However, the mean benefits of fungicide tended to decrease with increasing levels of genetic resistance, to the point that yield, disease, and gross margin benefits were close to zero in the most resistant cultivars. Overall, these findings suggest that fungicides can reduce blackleg severity, but the benefits of application strongly depend on associated levels of genetic resistance. Canola cultivars with higher genetic resistance reliably reduced blackleg disease and maintained grain yield without the associated cost of fungicide application. The intensification of canola production to meet increasing global demand will require strategies to sustainably manage and protect finite genetic resistance resources to control blackleg disease., Competing Interests: The author(s) declare no conflict of interest.

Blackleg is a worldwide disease of canola ( Brassica napus ), caused by a complex of fungal species in the genus Leptosphaeria , that impacts canola production and seed quality. Demethylation inhibitor (DMI) fungicides that target sterol 14α-demethylase are an integral part of disease control. Here, we report six DMI-resistant isolates of Leptosphaeria maculans and two different types of genetic modification related to the resistance. Analysis of the regulatory region of the DMI target gene ERG11 (also known as CYP51 ) revealed a 275-bp insertion in two of the isolates and three long terminal repeat retrotransposons (5,263, 5,267, and 5,248 bp) inserted in the promoter region of three resistant isolates. Genetic approaches confirmed that these elements are responsible for DMI resistance in L. maculans and crosses show segregation consistent with a single locus. Reverse-transcription quantitative PCR assays demonstrated that the 275-bp insertion increases ERG11 gene expression, conferring DMI fungicide resistance both in vitro and in planta. Moreover, transformation of a susceptible isolate of L. maculans with ERG11 driven by a promoter containing the 275-bp insertion increased resistance to tebuconazole. A minimal shift of the values of concentration whereby 50% of the mycelial growth is inhibited in vitro was observed in resistant isolates containing long terminal repeat retrotransposons; nevertheless, these isolates were able to develop significant lesions on cotyledons from fungicide-treated seedlings. This is the first report of genetic modifications in L. maculans relating to DMI fungicide resistance.

The infection by Leptosphaeria maculans of Brassica napus cultivars with major gene resistance derived from Brassica rapa subsp. sylvestris was studied in southeastern Australia. Following the commercial release of these cultivars in Australia in 2000, plants with stem cankers were first reported in 2002 at two geographically isolated regions in South Australia and New South Wales. In 2003, this study showed that the major gene resistance had been overcome in an area of approximately 50,000 ha in South Australia and in two fields in New South Wales (0.5 and 30 ha). There was no relationship between disease severity and incidence in 2003 and the proximity to the sites where resistance breakdown occurred in 2002. At some locations, the frequency of isolates able to overcome the B. rapa subsp. sylvestris-derived resistance had increased between 2002 and 2003. Isolates cultured from canola cultivars with either B. rapa subsp. sylvestris-derived resistance or polygenic resistance showed host specificity when inoculated onto cultivars with B. rapa subsp. sylvestris-derived or polygenic resistance, respectively. The most likely cause of the resistance breakdown was the rapid increase in frequency of L. maculans isolates virulent on this particular resistance source. The selection pressure leading to this increased frequency was probably mediated by the planting of cultivars harboring the major resistance gene in the same locations for a 3-year period, and the ability of the pathogen to produce large numbers of asexual and sexual spores.