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The Australian canola industry was established in the 1970s and has expanded since that time, particularly in the last two decades. This review addresses the changes in farming practices since the year 2000 and the epidemiological and management consequences for blackleg, caused by the fungus Leptosphaeria maculans, the main disease impacting Brassica napus production. To help understand the change in production practices, a survey of over 100 growers and agronomists was conducted. Modern management practices include increased crop residue retention, frequency of canola in crop sequences, number of resistance genes in cultivars, use of hybrids and fungicides as well as earlier sowing and flowering times. While some of the changes identified in the survey and in this review increase the risk and severity of disease, including new symptoms like upper canopy infection, others provide novel strategies for control. Keeping these changes in mind, a set of research priorities towards long term sustainable management of blackleg disease are identified. [ABSTRACT FROM AUTHOR]

Abstract: Genetic, physiological and physical homogenization of agricultural landscapes creates ideal environments for plant pathogens to proliferate and rapidly evolve. Thus, a critical challenge in plant pathology and epidemiology is to design durable and effective strategies to protect cropping systems from damage caused by pathogens. Theoretical studies suggest that spatio‐temporal variation in the diversity and distribution of resistant hosts across agricultural landscapes may have strong effects on the epidemiology and evolutionary potential of crop pathogens. However, we lack empirical tests of spatio‐temporal deployment of host resistance to pathogens can be best used to manage disease epidemics and disrupt pathogen evolutionary dynamics in real‐world systems. In a field experiment, we simulated how differences in Brassica napus resistance deployment strategies and landscape connectivity influence epidemic severity and Leptosphaeria maculans pathogen population composition. Host plant resistance, spatio‐temporal connectivity [stubble loads], and genetic connectivity of the inoculum source [composition of canola stubble mixtures] jointly impacted epidemiology (disease severity) and pathogen evolution (population composition). Changes in population composition were consistent with directional selection for the ability to infect the host (infectivity), leading to changes in pathotype (multilocus phenotypes) and infectivity frequencies. We repeatedly observed decreases in the frequency of unnecessary infectivity, suggesting that carrying multiple infectivity genes is costly for the pathogen. From an applied perspective, our results indicate that varying resistance genes in space and time can be used to help control disease, even when resistance has already been overcome. Furthermore, our approach extends our ability to test not only for the efficacy of host varieties in a given year, but also for durability over multiple cropping seasons, given variation in the combination of resistance genes deployed. [ABSTRACT FROM AUTHOR]

Blackleg, caused by Leptosphaeria maculans, is the main disease constraint for canola production in Australia. The fungus infects all aboveground and belowground parts of the canola plant. Yield loss in Australia and worldwide is generally associated with cankers at the crown, which arise from leaf infections during the early stages of seedling growth. Infection of flowers, peduncles, siliques, main stems and branches, with resultant lesions and canker formation, are typically uncommon symptoms. We propose the term 'upper canopy infection' to encompass symptoms on all of these plant parts because they generally occur together on the same plant and appear after the plant has undergone elongation. Branch and stem lesions observed in a commercial crop in 2010 were confirmed as L. maculans. Since then, assessment of upper canopy symptoms at 25 sites across the canola-producing regions of Australia between 2011 and 2016 show that symptoms are more prevalent, although they differed between sites and seasons. In 2011, symptoms were present at a single site, and this increased to seven sites in 2013 and 23 sites in 2016. Preliminary data indicate that infection arises from both ascospore and pycnidiospore inoculum, and that earlier onset of flowering is a key risk factor for more severe upper canopy infection. Evidence suggests that host genetic resistance may be an effective control for upper canopy infection. [ABSTRACT FROM AUTHOR]

Canola ( Brassica napus) crops for grazing and grain (dual-purpose) production provide an economic break-crop alternative for dual-purpose cereals in Australian mixed farming systems. Infection by Leptosphaeria maculans is the most prevalent disease in Australian canola crops with airborne inoculum released throughout the autumn and winter when crops are grazed. Glasshouse and field experiments were conducted to investigate the effect of mechanical defoliation (simulated grazing) on disease severity at plant maturity. In glasshouse experiments, stem canker severity increased from 4% to 24% in severely defoliated plants, but light defoliation had no effect compared with undefoliated control plants. Disease severity was increased with defoliation in all field experiments. Defoliation increased crown canker severity from 22.6% to 39.3% at Wagga Wagga and from 3.0% to 7.1% at Canberra and lodging from 9.6% to 11.9% at Naracoorte in the same set of cultivars assessed at each site. The increase in disease severity with defoliation was less in canola lines with moderate to high levels of stem canker resistance. Plants defoliated before stem elongation tended to develop less disease than those defoliated during the reproductive phase of plant growth. These findings suggest that the impact of grazing on L. maculans infection of canola crops can be minimised by sowing cultivars with a high level of stem canker resistance and grazing during the vegetative stage of plant growth prior to stem elongation. Further research is required to determine whether these management strategies are applicable in canola crops defoliated by grazing animals. [ABSTRACT FROM AUTHOR]

• To investigate the role played by the distribution pattern of glucosinolates (GSLs) in root systems in the release of biocides to the rhizosphere, GSLs have been localized, for the first time, to specific regions and cells in field-grown roots. • GSL concentrations in separated tissues of canola ( Brassica napus) were determined by chemical analysis, and cell-specific concentrations by extrapolation from sulphur concentrations obtained by quantitative cryo-analytical scanning electron microscopy (SEM). • In roots with secondary growth, GSL concentrations in the outer secondary tissues were up to 5× those of the inner core. The highest GSL concentrations (from sulphur measurements) were in two cell layers just under the outermost periderm layer, with up to 100× published concentrations for whole roots. Primary tissues had negligible GSL. • Release and renewal of the peripheral GSLs is probably a normal developmental process as secondary thickening continues and surface cells senesce, accounting for published observations that intact roots release GSLs and their biocide hydrolosates to the rhizosphere. Absence of myrosin idioblasts close to the root surface suggests that GSLs released developmentally are hydrolysed by myrosinase in the rhizosphere, ensuring a continuous localized source of biotoxic hydrolysates which can deter soil-borne pests, and influence microbial populations associated with long-lived components of the root system. [ABSTRACT FROM AUTHOR]

• Infection of Brassica napus cotyledons and leaves by germinating ascospores of Leptosphaeria maculans leads to production of leaf lesions followed by stem cankers (blackleg). Leptosphaeria maculans also causes root rot but the pathway of infection has not been described. • An L. maculans isolate expressing green fluorescent protein (GFP) was applied to the petiole of B. napus plants. Hyphal growth was followed by fluorescence microscopy and by culturing of sections of plant tissue on growth media. Leptosphaeria maculans grew within stem and hypocotyl tissue during the vegetative stages of plant growth, and proliferated into the roots within xylem vessels at the onset of flowering. Hyphae grew in all tissues in the stem and hypocotyl, but were restricted mainly to xylem tissue in the root. • Leptosphaeria maculans also infected intact roots when inoculum was applied directly to them and hyphae entered at sites of lateral root emergence. Hyphal entry may occur at other sites but the mechanism is uncertain as penetration structures were not observed. • Infection of B. napus roots by L. maculans can occur via above- and below-ground sources of inoculum, but the relative importance of the infection pathways under field conditions is unknown. [ABSTRACT FROM AUTHOR]

The Arabidopsis thaliana basic helix-loop-helix Leu zipper transcription factor (TF) MYC2/JIN1 differentially regulates jasmonate (JA)-responsive pathogen defense (e.g., PDF1.2) and wound response (e.g., VSP) genes. In this study, genomewide transcriptional profiling of wild type and mutant myc2/jin1 plants followed by functional analyses has revealed new roles for MYC2 in the modulation of diverse JA functions. We found that MYC2 negatively regulates Trp and Trp-derived secondary metabolism such as indole glucosinolate biosynthesis during JA signaling. Furthermore, MYC2 positively regulates JA-mediated resistance to insect pests, such as Helicoverpa armigera, and tolerance to oxidative stress, possibly via enhanced ascorbate redox cycling and flavonoid biosynthesis. Analyses of MYC2 cis binding elements and expression of MYC2-regulated genes in T-DNA insertion lines of a subset of MYC2-regulated TFs suggested that MYC2 might modulate JA responses via differential regulation of an intermediate spectrum of TFs with activating or repressing roles in JA signaling. MYC2 also negatively regulates its own expression, and this may be one of the mechanisms used in fine-tuning JA signaling. Overall, these results provide new insights into the function of MYC2 and the transcriptional coordination of the JA signaling pathway. [ABSTRACT FROM AUTHOR]