Disease Cycle
L. maculans has a complicated life cycle. The pathogen begins as a saprophyte on stem residue and survives in the stubble. It then begins its necrotrophic cycle by producing leaf spots. Colonizing the plant tissue systematically, it begins its endophytic stage. When the growing season ends, the fungus causes cankers beginning another necrotrophic stage.
L. maculans has both a teliomorph phase (ascospores) and an anamorph phase (pycnidia). 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.
Read more about this topic: Leptosphaeria Maculans
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