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1 nes, was present in all species of the genus Cochliobolus but absent in the filamentous fungus, Penic
2 ion cultures 3 to 5 h after inoculation with Cochliobolus carbonum (Race 1), and then increased rapid
3 determinant for the plant pathogenic fungus Cochliobolus carbonum and an inhibitor of histone deacet
4 Race 1 isolates of the filamentous fungus Cochliobolus carbonum are exceptionally virulent on cert
5 selective pathogenicity (TOX2) in the fungus Cochliobolus carbonum governs production of a cyclic tet
6 PsmES4326 infection, but not in response to Cochliobolus carbonum infection, indicating that PAD4 ha
7 hese include Cochliobolus heterostrophus and Cochliobolus carbonum infection, ultraviolet light treat
10 to confer resistance to the fungal pathogen Cochliobolus carbonum race 1, but the effectiveness of r
11 se inhibitor produced by the fungal pathogen Cochliobolus carbonum race 1, promotes virulence in maiz
12 sed by a previously unknown fungal pathogen, Cochliobolus carbonum race 1, was first described in 193
14 dopsis and leaves inoculated with the fungus Cochliobolus carbonum were fed [35S]cysteine (Cys) and [
15 S2, was isolated from the filamentous fungus Cochliobolus carbonum, a pathogen of maize that makes th
16 ccSNF1, was isolated from the maize pathogen Cochliobolus carbonum, and ccsnf1 mutants of HC toxin-pr
17 chitooligosaccharides, and by infection with Cochliobolus carbonum, Cochliobolus heterostrophus and F
19 , caused by the necrotrophic fungal pathogen Cochliobolus heterostrophus (anamorph Bipolaris maydis),
21 and by infection with Cochliobolus carbonum, Cochliobolus heterostrophus and Fusarium verticillioides
22 determinant in the maize (Zea mays) pathogen Cochliobolus heterostrophus and is involved in tolerance
23 genes from the related heterothallic species Cochliobolus heterostrophus can also influence U. botryt
24 Inoculation with the nonpathogenic fungus Cochliobolus heterostrophus drastically reduced the ligh
25 as a virulence factor in the maize pathogen Cochliobolus heterostrophus Hypothesizing that the homol
28 like kinase gene which we have called ChSK1 (Cochliobolus heterostrophus Susceptibility Kinase 1) at
29 rtional mutants of the fungal maize pathogen Cochliobolus heterostrophus were screened for altered vi
30 bacteria (Ralstonia solanacearum) and fungi (Cochliobolus heterostrophus) results in reduced virulenc
31 ght (SLB), caused by the necrotrophic fungus Cochliobolus heterostrophus, is a major foliar disease o
33 controlling the difference between races of Cochliobolus heterostrophus: race T is highly virulent o
36 thologs in the rice (Oryza sativa) pathogen, Cochliobolus miyabeanus, the wheat (Triticum aestivum) p
37 sequences from homothallic and heterothallic Cochliobolus species support the hypothesis that heterot
38 in varying copy number in the genomes of all Cochliobolus spp. examined, giving a distinct fingerprin
41 entification of susceptibility to the fungus Cochliobolus victoriae in Arabidopsis thaliana has enabl
42 and race O of C. heterostrophus on maize, of Cochliobolus victoriae on oats, and of Gibberella zeae o
43 effector produced by the necrotrophic fungus Cochliobolus victoriae), TRX-h5 (a defense-associated th
44 ctorin, the host-selective toxin produced by Cochliobolus victoriae, the causal agent of victoria bli
45 ctorin is a host-selective toxin produced by Cochliobolus victoriae, the causal agent of victoria bli
46 f Avena sativa (oat) is caused by the fungus Cochliobolus victoriae, which is pathogenic because of t
47 rom the filamentous fungus Helminthosporium (Cochliobolus) victoriae that copurifies with mycoviral d