Leptosphaeria maculans (anamorph Phoma lingam) is a fungal pathogen of the phylum Ascomycota that is the causal agent of blackleg disease on Brassica crops. Its genome was one of the original plant pathogens that were sequenced using Sanger chemistry coupled with physical and genetic maps, indicative that L. maculans is a well-studied model phytopathogenic fungus. Most research focused on disease and its prevention. Symptoms of blackleg disease generally include basal stem cankers, small grey lesions on leaves, and root rot. The major yield loss is due to stem canker. The fungus is dispersed by the wind as ascospores or rain splash in the case of the conidia. L. maculans grows best in wet conditions and a temperature range of 5–20 degrees Celsius. Rotation of crops, removal of stubble, application of fungicide, and crop resistance are all used to manage blackleg. The fungus is an important pathogen of Brassica napus (canola) crops.
Host and symptoms Leptosphaeria maculans causes phoma stem canker or blackleg. Symptoms generally include basal stem cankers, small grey oval lesions on the leaf tissue and root rot (as the fungus can directly penetrate roots). L. maculans infects a wide variety of Brassica crops including cabbage (Brassica oleracea) and oilseed rape (Brassica napus). L. maculans is especially virulent on Brassica napus. The first dramatic epidemic of L. maculans occurred in Wisconsin on cabbage. The disease is diagnosed by the presence of small black pycnidia which occur on the edge of the leaf lesions. The presence of these pycnidia allow for this disease to be distinguished from Alternaria brassicae, another foliar pathogen with similar lesions, but no pycnidia.
Disease cycle Leptosphaeria maculans has a complicated life cycle. The pathogen begins as a saprophyte on stem residue and survives in the stubble. It then begins a hemibiotrophic stage that results in the production of leaf spots. Colonizing the plant tissue systemically, it begins its endophytic stage within the stem. (Due to its systemic parasitism, quantitative assessment of L. maculans's impact cannot include lesion size or number.) When the growing season ends, the fungus causes cankers at the base of the plant thereby beginning another necrotrophic stage. Leptosphaeria maculans has both a teleomorph phase (sexual reproduction to generate pseudothecia that release ascospores) and an anamorph phase (asexual reproduction to produce pycnidia that release pycnidiospores). The disease spreads by wind born dispersal of ascospores and rain splash of conidia. In addition, phoma stem canker can also be spread by infected seeds when the fungus infects the seed pods of Brassica napus during the growing season, but this is far less frequent. The disease is polycyclic in nature even though the conidia are not as virulent as the ascospores. The disease cycle starts with airborne ascospores which are released from the pseudothecia in the spring. The ascospores enter through the stomata to infect the plant. Soon after the infection, gray lesions and black pycnidia form on the leaves. During the growing season, these pycnidia produce conidia that are dispersed by rain splash. These spores cause a secondary infection which is usually less severe than primary infection with ascospores. Stem cankers form from the disease moving systemically through the plant. Following the colonization of the intercellular spaces, the fungus will reach a vascular strand and spread down the stalk between the leaf and the stem. The disease will spread into as well as between the cells of the xylem. This colonization leads to the invasion and destruction of the stem cortex, which leads to the formation of stem canker. Stubble forms after the growing season due to residual plant material left in the field after harvest. The disease overwinters as pseudothecia and mycelium in the stubble. In spring the pseudothecia release their ascospores and the cycle repeats itself.
Impact of environment on reproduction Temperature and moisture are the two most important environmental conditions for the development of L. maculans spores. A temperature of 5-20 degrees Celsius is the optimal temperature range for pseudothecia to mature. A wet humid environment increases the severity of the disease due to the dispersal of conidia by rain splash. As well as rain, hail storms also increase the severity of the disease.
Management of disease Cultural methods such as removing stubble and crop rotation can be very effective. By removing the stubble, overwintering pseudothecia and mycelium are less prevalent, reducing the risk of infection. In Canada, crop rotation decreases blackleg dramatically in canola crops. It is suggested to have a 3-year crop rotation of canola and to plant non-host plants such as cereals in between these periods. Application of fungicides decrease disease symptoms, although usage varies in growing regions and conditions. Demethylation inhibitor (DMI) fungicides are the most extensively used. DMI fungicides inhibit ergosterol biosynthesis. DMI fungicides function on L. maculans as they inhibit the growth of conidia and mycelia, though they have no effect on ascospores which will grow regardless of the fungicide concentration. However, changes in the gene encoding the protein targeting the DMI fungicides in Australia and Europe raises concerns about their ongoing ability to control disease. Another major class of fungicides being used are the succinate dehydrogenase inhibitors (SDHIs), which target mitochondrial function. Resistance methods due to genes present within the plant can be used to great effect in mitigating disease. Typically race specific Rlm genes are used for resistance (Rlm1-Rlm9) in Brassica napus crops. These are described in more detail below.
Plant disease resistance Leptosphaeria maculans is controlled by both race-specific gene-for-gene resistance via so-called resistance (R) genes detecting corresponding avirulence (Avr) genes and quantitative, broad, resistance traits. Since the L. maculans genome was sequenced and due to the importance of this pathogen, many different Avr genes have been sought and identified.
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