There are three main sources of infection: nearby infected seeds, spores from plant debris in the topsoil and Brassica weeds, and spores moved by wind and air from farther away. Infected leaves can spread their spores up to a diameter of 1800m. There are also three major entry points to the host cell:
epidermal penetration,
stomatal penetration and penetration through an insect. Contact with the host cell triggers the release of various cell wall degrading enzymes which allow the fungus to attach itself to the plant and begin degradation. The suggested mode of attack is through host-specific toxins, primarily
AB toxins, that induce cell death by
apoptosis. This results in what look like dents and lesions in the host plant. These are brown, concentric circles with a yellow tinge at the circumference, usually about 0.5-2.5 cm in diameter.
Necrosis can generally be observed within 48 hours of infection. The spores can reside on the external seed coat of infected seeds, but the
mycelium can also penetrate under the seed coat, where it has the ability to remain viable for several years. Occasionally, it can even penetrate the
embryo tissue. The primary mode of transmission is through contaminated seed. Also, the infection is not limited to specific areas of the host plant; it can spread all over and even cause
damping off of the seedlings at a relatively early stage. It also affects the host species at various developmental stages. As mentioned above, seedlings exhibit dark stem lesions followed by damping off. Velvety, black spots, resembling soot, can be observed on older plants. Pathogenesis is affected by factors such as: temperature, humidity, pH, reactive oxidation species, host defense molecules.
Genes Out of the 10,688 predicted
genes from the
A. brassicicola genome, 139 encode small secretion proteins that may be involved in pathogenesis, 76 encode
lipases and 249 encode
glycosyl hydrolases that are important for
polysaccharide digestion, potentially damaging host cells. In contrast, mutations in genes such as
AbHog1,
AbNPS2, and
AbSlt2 affect cell wall integrity and make the fungus more susceptible to host defenses. Currently, research is being done to identify the gene(s) responsible for encoding a
transcription factor, Bdtf1, important for the detoxification of host
metabolites.
Biochemistry The most common toxin studied for
A. brassicicola is the AB toxin, said to be connected to the
virulence,
pathogenicity and host range for the fungus. It is most likely produced during conidial germination and probably linked to the ability of the fungus to infect and colonize Brassica leaves However, recent studies have explored new potential metabolites. For example, this fungus also produces
histone deacetylase inhibitors, but these do not have a significant impact on lesion size. Some studies show only a 10% reduction in virulence. Furthermore,
alternariol and
tenuazonic acid seem to affect mitochondrial-mediated apoptosis pathways and protein synthesis respectively (in the host cell), but again, not to a significant degree. Some
cytokines have been linked with the discolouration associated with
A. brassicicola infection. Cell wall degrading enzymes like
lipases and
cutinases are also linked to its pathogenicity, but more evidence of their efficacy is required. One important transcription factor is AbPf2. It regulates 6 of the 139 genes encoding small secretion proteins and may have a role in pathogenesis, specifically cellulose digestion.
Treatments In order to protect their crops, many individuals pre-treat their seeds with
fungicides. The most widespread active ingredients in these fungicides are
Iprodione and
Strobilurins. In 1995, it was reported that Iprodione most likely acts by mutating two
histidine residues in the target site of enzymes. Ultimately, it inhibits germ tube growth. However, the ubiquitous use of fungicides has resulted in the fungus growing increasingly resistant. Thus, different, non-chemical approaches have been explored. People have tried to develop resistant
Brassicaceae crops through breeding. However, this has proved challenging due to the difficulty of transferring genes from wild-type to cultivated strains, resulting in
genetic bottlenecks. It is further complicated by the probability that resistance seems to be a
polygenic trait. There are also some
Brassica plants that have developed resistance to the pathogen naturally. High
phenolase activity, high leaf sugar, and thicker wax layers reduce water-borne spore germination. It has been shown that the presence of
camalexin in the host plant helps it to disrupt pathogen development. For example, an Arabidopsis mutant in the
pad-3 gene that does not produce camalexin is more susceptible to infection. Varying levels show differing levels of resistance. Another suggestion put forth is crop debris management. The aim is to minimize exposure of the crop plants to spores present in the soil by using crop rotation and weed control. Biological approaches have also been studied. One approach has been to use antagonistic fungi such as
Aureobasidium pullulans &
Epicoccum nigrum to subdue the effect of
A. brassicicola. The plants
C. fenestratum and
Piper betle also show potent fungicidal activity towards
A. brassicicola both in vitro and under greenhouse conditions. These levels are comparable to Iprodione. The active compound,
berberine, affects cell wall integrity and
ergosterol biosynthesis. Ethanol extracts from the dried roots of
Solanum nigrum (black nightshade), traditionally used as herbal remedies in places ranging from the Far East to
India and
Mexico, show promising anti-fungal activity as well. They seem to suppress conidial germination, possibly by interfering with the AB toxin. == Economic impact ==