Alternaria brassicicola

Alternaria brassicicola is a fungal necrotrophic plant pathogen that

causes black spot disease on a wide range of hosts, particularly in Alternaria brassicicola
the genus of Brassica, including a number of economically
important crops such as cabbage, Chinese cabbage, cauliflower,
oilseeds, broccoli and canola.[1][2][3] Although mainly known as a
significant plant pathogen, it also contributes to various respiratory
allergic conditions such as asthma and rhinoconjunctivitis.[4]
Despite the presence of mating genes, no sexual reproductive stage
has been reported for this fungus.[5][1][3] In terms of geography, it is
most likely to be found in tropical and sub-tropical regions, but also
in places with high rain and humidity such as Poland.[3] It has also
been found in Taiwan and Israel.[6][7] Its main mode of propagation Scientific classification
is vegetative. The resulting conidia reside in the soil, air and Kingdom: Fungi
water.[3] These spores are extremely resilient and can overwinter on
crop debris and overwintering herbaceous plants.[3] Division: Ascomycota
Class: Dothideomycetes
Order: Pleosporales
Contents
Family: Pleosporaceae
Growth and morphology
Genus: Alternaria
Research history
Growth cycle Species: A. brassicicola

Pathogenesis and infection Binomial name

Genes Alternaria brassicicola
Biochemistry (Schwein.) Wiltshire, (1947)
Treatments
Synonyms
Economic impact
References Alternaria brassicae f. microspora
Alternaria brassicae var. minor
Alternaria circinans Berk. & M.A.
Growth and morphology Curtis, (1924)
Alternaria oleracea Milbraith,
The conidia of A. brassicicola are abundant in the outdoor (1922)
environment from the months of May to late October in the northern Helminthosporium brassicae
hemisphere, peaking in June and again in October.[4] The conidia Henn, (1902)
are dark brown[8] and smooth-walled, up to 60 x 14µm.[9][2] The Helminthosporium brassicicola
conidia are cylindrical to oblong in shape and are muriform and Schwein, (1832)
produced in chains of 8-10 spores.[9] They are firmly attached to Macrosporium cheiranthi var.
circinans Berk. & M.A. Curtis, (1875)
conidiophores[4] that are olive-brown, septate, and growing to an
Macrosporium circinans
upper range of 100-200 µm, although this overall length may
Macrosporium commune var.
vary.[8] Conidia are borne in continuous, chain-like structure, but
circinans
branching at the base has also been observed.[2] Although conidia
Polydesmus exitiosus f.
can be spread by rain, the most common means of spread is through
the air.[4] The fungus grows on epidermal leaf wax of plants, alternarioides J.G. Kühn, (1855)
particularly those in the Brassicaceae, and prefers an environment Polydesmus exitiosus f.
with high humidity and temperature range of 20–30 °C (68– luxuriosum
86 °F).[3] Macroscopically, the mycelium exhibits a range of colour: Sporidesmium exitiosum f.
unpigmented when young, to olive-grey, grey-black at alternarioides
maturity.[9][2] Colonies of A. brassicicola tend to be dark brown or Sporidesmium exitiosum f.
black in colour.[2] luxuriosum
Sporidesmium septorioides

Research history
Historically, much of the early research
concerning the fungus was based on
plant defense mechanisms. However,
once its genome was sequenced, efforts
shifted to identifying the genes involved
in host-parasite interaction.[1] One of the
pioneers for genetic research into
Alternaria brassicicola was the Alternaria brassicicola chain-like conidia (left and right)
Lawrence group at Virginia
Bioinformatics Institute and the Genome
Center at Washington University.[1] The
most common media used for A.
brassicicola growth are PDA (potato
dextrose agar) and V8 juice-agar. In
vitro and under optimal conditions,
colonies grow rapidly and appear dark
green or white-grey. Spontaneous
sporulation occurs at 25ºC in darkness
on PDA medium.[3]
Legions of A. brassicicola on Chinese Kale

Growth cycle

Hours after inoculation:

2h: Conidia swells

3h: Germ tube formation observed at the apical or
middle cells of conidia
8h: Vesicle of dissolved contents moves from conidial
cell to germ tube
20h: Infection of the host cell
48h: Mycelial network develops on the surface
72h: Many chains of conidia can be seen [5] Colonies of A. brassicicola on Potato
Dextrose Agar after 3 d (l) and 7 d (r).

Pathogenesis and infection

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.[3] 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.[3] 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.[10] The suggested mode of attack is through host-specific toxins, primarily AB toxins, that induce
cell death by apoptosis.[3] This results in what look like dents and lesions in the host plant.[3] These are brown,
concentric circles with a yellow tinge at the circumference, usually about 0.5-2.5cm in diameter.[11][5][1]
Necrosis can generally be observed within 48 hours of infection.[11] 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.[1] Occasionally, it can even penetrate the embryo tissue.[6] The primary mode
of transmission is through contaminated seed.[5] 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.[3] It also
affects the host species at various developmental stages.[9] As mentioned above, seedlings exhibit dark stem
lesions followed by damping off. Velvety, black spots, resembling soot, can be observed on older plants.[9]
Pathogenesis is affected by factors such as: temperature, humidity, pH, reactive oxidation species, host defense
molecules.[3]

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.[1]

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.[3] It is most likely produced during conidial germination and
probably linked to the ability of the fungus to infect and colonize Brassica leaves [10] 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.[3] Some studies show only a 10%
reduction in virulence.[1] 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.[3] Cell wall
degrading enzymes like lipases and cutinases are also linked to its pathogenicity, but more evidence of their
efficacy is required.[1] 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.[1]

Treatments

In order to protect their crops, many individuals pre-treat their seeds with fungicides.[3] The most widespread
active ingredients in these fungicides are Iprodione and Strobilurins.[3] In 1995, it was reported that Iprodione
most likely acts by mutating two histidine residues in the target site of enzymes.[5] Ultimately, it inhibits germ
tube growth.[6] However, the ubiquitous use of fungicides has resulted in the fungus growing increasingly
resistant.[6] 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.[3]
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.[3]

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.[3] 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.[6] 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.[7]

Economic impact
As mentioned previously, Alternaria brassicicola causes severe black spot diseases in a number of
ecologically important crops. Often, it occurs in conjunction with Alternaria brassicae. However, it is the more
dominant invasive species. These infections lead to a significant loss in viable seeds and produce. The
resulting lesions greatly reduce available photosynthetic area, leading to wilt and plant death. Crops like
infected cabbages do not last long during storage or transportation.[3] In some cases, yield reductions can be as
high as 20-50%.[1] The lack of ability to use fungicides makes it challenging to sustain organic crops in a cost-
effective way.[10]

References
1. Cho, Yangrae (April 2015). "How the Necrotrophic Fungus Alternaria brassicicola Kills Plant
Cells Remains an Enigma" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4385798).
Eukaryotic Cell. 14 (4): 335–344. doi:10.1128/EC.00226-14 (https://doi.org/10.1128%2FEC.00
226-14). PMC 4385798 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4385798).
PMID 25681268 (https://pubmed.ncbi.nlm.nih.gov/25681268).
2. Ellis, M.B (1968). "Alternaria brassicicola". CMI Descriptions of Pathogenic Fungi and Bacteria.
163.
3. Nowicki, Marcin; et al. (30 August 2012), "Alternaria black bot of crucifers: Symptoms,
importance of disease, and perspectives of resistance breeding" (http://www.degruyter.com/vie
w/j/vcrb.2012.76.issue--1/v10032-012-0001-6/v10032-012-0001-6.xml), Vegetable Crops
Research Bulletin, 76, doi:10.2478/v10032-012-0001-6 (https://doi.org/10.2478%2Fv10032-01
2-0001-6), retrieved 2012-09-01
4. Fernández-Rodríguez, Santiago (15 Nov 2015). "Potential sources of airborne Alternaria spp.
spores in South-west Spain". Science of the Total Environment. 533: 165–176.
Bibcode:2015ScTEn.533..165F (https://ui.adsabs.harvard.edu/abs/2015ScTEn.533..165F).
doi:10.1016/j.scitotenv.2015.06.031 (https://doi.org/10.1016%2Fj.scitotenv.2015.06.031).
PMID 26156135 (https://pubmed.ncbi.nlm.nih.gov/26156135).
5. Macioszek, V. K.; Lawrence, C. B.; Kononowicz, A. K. (June 2018). "Infection cycle of Alternaria
brassicicola on Brassica oleracea leaves under growth room conditions". Plant Pathology. 67
(5): 1088–1096. doi:10.1111/ppa.12828 (https://doi.org/10.1111%2Fppa.12828).
S2CID 90987400 (https://api.semanticscholar.org/CorpusID:90987400).
6. Huang, Ruguo (1995). "Characterization of Iprodione-resistant isolates of Alternaria
brassicicola". Plant Dis. 79 (8): 828–833. doi:10.1094/pd-79-0828 (https://doi.org/10.1094%2Fp
d-79-0828).
 7. Muto, Machiko (2005). "Control of Black Leaf Spot (Alternaria brassicicola) of Crucifers by
Extracts of Black Nightshade (Solanum nigrum)". Plant Pathology Bulletin. 14: 25–34.
8. Simmons, Emory (2007). An Identification Manual. CBS Fungal Diversity Centre.
9. Meena, P.D (2010). "Alternaria blight: a chronic disease in rapeseed-mustard". Journal of
Oilseed Brassica. 1 (1): 1–11.
10. Amein, Tahsein (December 2011). "Evaluation of non-chemical seed treatment methods for
control of Alternaria brassicicola on cabbage seeds". Journal of Plant Diseases and Protection.
118 (6): 214–221. doi:10.1007/bf03356406 (https://doi.org/10.1007%2Fbf03356406).
S2CID 86825188 (https://api.semanticscholar.org/CorpusID:86825188).
11. Dethoup, Tida (September 2018). "Fungicidal activity of Thai medicinal plant extracts against
Alternaria brassicicola causing black spot of Chinese kale". European Journal of Plant
Pathology. 152 (1): 157–167. doi:10.1007/s10658-018-1460-5 (https://doi.org/10.1007%2Fs106
58-018-1460-5). S2CID 51886893 (https://api.semanticscholar.org/CorpusID:51886893).

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