Leptosphaeria maculans

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 has been sequenced, and L. maculans is a well-studied model phytopathogenic fungus. Symptoms of blackleg 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. L. 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. L. 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 systematically, it begins its endophytic stage within the stem. When the growing season ends, the fungus causes cankers at the base of the plant thereby beginning another necrotrophic stage. L. 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.