The filamentous ascomycete genus Cochliobolus (anamorph
Bipolaris/Curvularia) is comprised of more than
forty closely related species, some of which are highly aggressive,
superpathogens with particular specificity to their host plants.
All members of the genus known to cause serious crop diseases fall
in a tight phylogenetic group suggesting that a progenitor within
the genus gave rise, over a relatively short period of time to the
series of distinct biotypes (1), each distinguished by unique
pathogenic capability to individual types of cereal.
Aggressive members include the necrotrophic corn pathogens
Cochliobolus heterostrophus and Cochliobolus
carbonum, the oat pathogen, Cochliobolus victoriae,
the rice pathogen, Cochliobolus miyabeanus, the sorghum
pathogen, Bipolaris sorghicola, the sugarcane pathogen,
Bipolaris sacchari and the hemibiotrophic generalized
cereal and grass pathogen, Cochliobolus
sativus.
The interaction between rice and C. miyabeanus is
inadequately understood from the perspective of genetic and
molecular mechanisms, although it has been reported that, like
other Cochliobolus species, the fungus utilizes
phytotoxins to trigger host cell death (2). Other necrotrophic
Cochliobolus spp. and related taxa (e.g., Pyrenophora
tritici repentis, Stagonospora nodorum,
Alternaria alternata), are notorious for their ability to
evolve novel, highly virulent, races producing Host Selective
Toxins (HSTs). In contrast, no HST has been correlated with the
ability of C. miyabeanus (anamorph: Bipolaris
oryzae) to cause brown spot disease of rice. C.
miyabeanus does produce several secondary metabolites that act
as non-specific phytotoxins, including Ophiobolins A and B and
rapid cell death results when rice cultivar Nakdong is inoculated
with conidial germination fluid, suggesting production of a
phytotoxin (2). Nowadays, brown spot is widespread and the disease
along with sheath blights (Rhizoctonia solani), account
for the highest yield loss in south and Southeast Asia (3, 4).
Disease symptoms develop gradually and emerge as small purple brown
spots that later enlarge into oval lesions with brown necrotic
centers that are frequently surrounded by chlorotic halos (5, see
image). Under conducive circumstances in the field, the disease can
become polycyclic because C. miyabeanus has the potential to
complete its asexual cycle in 10–14 days (6). The sexual
stage of C. miyabeanus is similar to that of heterothallic
C. heterostrophus. Both mating types can be found in the
field (7).
1. Berbee ML, Pirseyedi M, Hubbard S (1999)
Cochliobolus phylogenetics and the origin of known, highly virulent
pathogens, inferred from ITS and glyceraldehyde-3-phosphate
dehydrogenase gene sequences. Mycologia 91: 964-977.
2. Ahn I-P, Kim S, Kang S, Suh S-C, Lee Y-H
(2005) Rice defense mechanisms against Cochliobolus miyabeanus and
Magnaporthe grisea are distinct. Phytopathology 95:
1248-1255.
3. Xiao JZ, Tsuda M, Doke N, Nishimura S
(1991) Phytotoxins produced by germinating spores of Bipolaris
oryzae. Phytopathology 81: 58–64.
4. Savary S, Willocquet L, Elazegui FA, Castilla
NP, Teng PS (2000a) Rice pest constraints in tropical Asia:
quantification of yield losses due to rice pests in a range of
production situations. Plant Disease 84: 357–369.
5. Savary S, Willocquet L, Elazegui FA, Teng PS,
Du PV, Zhu D, Tang Q, Huang S, Lin X, Singh HM, (2000b) Rice pest
constraints in tropical Asia: characterization of injury profiles
in relation to production situations. Plant Dis 84:
341–356.
6. Johnson DR, Percich JA, (1992). Wildrice
domestication, fungal brown spot disease and the future of
commercial production in Minnesota. Plant Disease 76:
1193–8.
7. Castell-Miller CV, Samac DA (2012).
Population genetic structure, gene flow and recombination of
Cochliobolus miyabeanus on cultivated wildrice (Zizania palustris).
Plant Pathology DOI: 10.1111/j.1365-3059.2011.02581.x
Genome Reference(s)
Condon BJ, Leng Y, Wu D, Bushley KE, Ohm RA, Otillar R, Martin J, Schackwitz W, Grimwood J, MohdZainudin N, Xue C, Wang R, Manning VA, Dhillon B, Tu ZJ, Steffenson BJ, Salamov A, Sun H, Lowry S, LaButti K, Han J, Copeland A, Lindquist E, Barry K, Schmutz J, Baker SE, Ciuffetti LM, Grigoriev IV, Zhong S, Turgeon BG
Comparative genome structure, secondary metabolite, and effector coding capacity across Cochliobolus pathogens.
PLoS Genet. 2013;9(1):e1003233. doi: 10.1371/journal.pgen.1003233