Symptoms of blackleg generally include basal stem cankers, small grey lesions on leaves, and root rot.

[4] The disease is diagnosed by the presence of small black pycnidia which occur on the edge of the leaf lesions.

(Due to its systemic parasitism, quantitative assessment of L. maculans's impact cannot include lesion size or number.

)[6] When the growing season ends, the fungus causes cankers at the base of the plant thereby beginning another necrotrophic stage.

The disease spreads by wind born dispersal of ascospores and rain splash of conidia.

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.

[7] Stubble forms after the growing season due to residual plant material left in the field after harvest.

[10] A wet humid environment increases the severity of the disease due to the dispersal of conidia by rain splash.

By removing the stubble, overwintering pseudothecia and mycelium are less prevalent, reducing the risk of infection.

Typically race specific Rlm genes are used for resistance (Rlm1-Rlm9) in Brassica napus crops.

Since L. maculans is sequenced [2] and due to the importance of this pathogen, many different Avr genes have been identified and cloned.

Arabidopsis thaliana is a commonly used model organism in plant sciences which is closely related to Brassica.

Interestingly, this model organism shows a very high degree of resistance to L. maculans in all accessions tested (except An-1, which provided the source for the rlm3 allele, see below) with no known virulent races known to date, which makes this pathosystem close to a non-host interaction.

[17] In contrast to RLM1 and RLM2 , RLM3 is not specific to L. maculans and mutant alleles in this gene cause broad susceptibility to multiple fungi.

[15] On the other hand, are mutants disrupted in abscisic acid (ABA) biosynthesis or signaling susceptible to L.

Most resistance traits have been introgressed into B. napus from wild Brassica rapa (AA genome) relatives.

In contrast, none or very few L. maculans resistance traits can be found in the Brassica oleracea (CC genome) parental species.

[24] The Rlm2 gene encodes for a receptor-like protein with a transmembrane domain and extracellular leucine rich repeats.

Leptosphaeria maculans is the most damaging pathogen of Brassica napus, which is used as a feed source for livestock and for its rapeseed oil.

The most recent significant losses were in 2003, to the widely planted B. napus cultivars containing a resistance gene from B.

[30] L. maculans metabolizes brassinin, an important phytoalexin produced by Brassica species, into indole-3-carboxaldehyde and indole-3-carboxylic acid.

[33] As a bioengineering innovation, in 2010 it was shown that a light-driven protein from L. maculans could be used to mediate, alongside earlier reagents, multi-color silencing of neurons in the mammalian nervous system.