Susceptibility to Leaf Blight, caused by Cochliobolus heterostrophus, in Nigerian Varieties of Maize

Nature ◽  
1961 ◽  
Vol 191 (4787) ◽  
pp. 515-516 ◽  
Author(s):  
C. L. M. VAN EIJNATTEN
Keyword(s):  
Leaf Blight ◽  
Cochliobolus Heterostrophus

Cochliobolus heterostrophus. [Descriptions of Fungi and Bacteria].

1971 ◽  
Author(s):  
M. B. Ellis
Keyword(s):  
Zea Mays ◽  
Geographical Distribution ◽  
Leaf Sheath ◽  
Leaf Blight ◽  
Disease Spread ◽  
Cochliobolus Heterostrophus ◽  
Sorghum Vulgare ◽  
Main Host ◽  
The Tropics ◽  
Diffuse Lesion

Abstract A description is provided for Cochliobolus heterostrophus. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Generally on leaves of Zea mays, the main host, Euchlaena mexicana, Sorghum vulgare and many species of Gramineae (41: 40; 45, 3084; 48, 414; 50, 2257i). During an epidemic in USA caused by race T in 1970 no important hosts apart from Z. mays were noted (50, 2257b). DISEASE: Southern leaf blight of maize, forming very numerous lesions up to 2.5 cm long, mostly on the leaves. They are at first elliptical, then longitudinally elongate, becoming rectangular as restriction by the veins occurs; cinnamon-buff (sometimes with a purplish tint) with a reddish-brown margin and occasionally zonate, coalescing and becoming greyish with conidia. Symptoms caused by race T show a less well defined, somewhat diffuse lesion, with marginal chlorosis leading to leaf collapse, and all parts of the plant can be attacked. Perithecia have been recently reported in the field at the junction of leaf sheath and blade (50, 2257j). GEOGRAPHICAL DISTRIBUTION: Widespread in the tropics and subtropics (CMI Map 346, ed. 3, 1969) but not reported from Australia. Records not yet mapped are: Brunei, Guatemala, Hawaii, Israel, Laos, Mexico, Salvador and Venezuela. TRANSMISSION: Presumably air-dispersed but no detailed studies seem to have been reported. During the recent USA outbreak the disease spread from Florida to Maine in c. 6 months (50, 2257c). Spread by seed occurs (50, 3690, 3692; Crosier & Boothroyd, Phytopathology 61: 427, 747).

scholarly journals First Report of Southern Leaf Blight Caused by Cochliobolus heterostrophus on Corn (Zea mays) in Fujian Province, China

Plant Disease ◽  
2016 ◽  
Vol 100 (8) ◽  
pp. 1781 ◽  
Author(s):  
Y. L. Dai ◽  
X. J. Yang ◽  
L. Gan ◽  
F. R. Chen ◽  
H. C. Ruan ◽  
...  
Keyword(s):  
Zea Mays ◽  
Leaf Blight ◽  
Cochliobolus Heterostrophus ◽  
Fujian Province ◽  
First Report ◽  
Southern Leaf Blight

scholarly journals Clues to an Evolutionary Mystery: The Genes for T-Toxin, Enabler of the Devastating 1970 Southern Corn Leaf Blight Epidemic, Are Present in Ancestral Species, Suggesting an Ancient Origin

2018 ◽  
Vol 31 (11) ◽  
pp. 1154-1165 ◽  
Author(s):  
Bradford J. Condon ◽  
Candace Elliott ◽  
Jonathan B. González ◽  
Sung Hwan Yun ◽  
Yasunori Akagi ◽  
...  
Keyword(s):  
United States ◽  
Phylogenetic Analyses ◽  
Leaf Blight ◽  
Cochliobolus Heterostrophus ◽  
Eastern United States ◽  
Genome Sequences ◽  
Evolutionary Origins ◽  
Biological Specificity ◽  
Protein Tree ◽  
Corn Leaf Blight

The Southern corn leaf blight (SCLB) epidemic of 1970 devastated fields of T-cytoplasm corn planted in monoculture throughout the eastern United States. The epidemic was driven by race T, a previously unseen race of Cochliobolus heterostrophus. A second fungus, Phyllosticta zeae-maydis, with the same biological specificity, appeared coincidentally. Race T produces T-toxin, while Phyllosticta zeae-maydis produces PM-toxin, both host-selective polyketide toxins necessary for supervirulence. The present abundance of genome sequences offers an opportunity to tackle the evolutionary origins of T- and PM- toxin biosynthetic genes, previously thought unique to these species. Using the C. heterostrophus genes as probes, we identified orthologs in six additional Dothideomycete and three Eurotiomycete species. In stark contrast to the genetically fragmented race T Tox1 locus that encodes these genes, all newly found Tox1-like genes in other species reside at a single collinear locus. This compact arrangement, phylogenetic analyses, comparisons of Tox1 protein tree topology to a species tree, and Tox1 gene characteristics suggest that the locus is ancient and that some species, including C. heterostrophus, gained Tox1 by horizontal gene transfer. C. heterostrophus and Phyllosticta zeae-maydis did not exchange Tox1 DNA at the time of the SCLB epidemic, but how they acquired Tox1 remains uncertain. The presence of additional genes in Tox1-like clusters of other species, although not in C. heterostrophus and Phyllosticta zeae-maydis, suggests that the metabolites produced differ from T- and PM-toxin.

scholarly journals Identification and Mapping of Quantitative Trait Loci Conditioning Resistance to Southern Leaf Blight of Maize Caused by Cochliobolus heterostrophus Race O

2004 ◽  
Vol 94 (8) ◽  
pp. 862-867 ◽  
Author(s):  
M. L. Carson ◽  
C. W. Stuber ◽  
M. L. Senior
Keyword(s):  
Quantitative Trait Loci ◽  
Quantitative Trait ◽  
Leaf Blight ◽  
Chromosome 1 ◽  
Cochliobolus Heterostrophus ◽  
Phenotypic Variance ◽  
Polygenic Inheritance ◽  
Trait Loci ◽  
Southern Leaf Blight ◽  
Ri Lines

A random set of recombinant inbred (RI) lines (F2:7) derived from the cross of the inbred lines Mo17 (resistant) and B73 (susceptible) were evaluated for resistance to southern leaf blight (SLB) caused by Cochliobolus heterostrophus race O. The RI lines were genotyped at a total of 234 simple sequence repeat, restriction fragment length polymorphism, or isozyme loci. Field plots of the RI lines were inoculated artificially with an aggressive isolate of C. heterostrophus race O in each of two growing seasons in North Carolina. Lines were rated for percent SLB severity two (1996) or three (1995) times during the grain-filling period. Data also were converted to area under the disease progress curve (AUDPC) and analyzed using the composite interval mapping option of the PLABQTL program. When means of disease ratings over years were fitted to models, a total of 11 quantitative trait loci (QTLs) were found to condition resistance to SLB, depending upon which disease ratings were used in the analyses. When the AUDPC data were combined and analyzed over environments, seven QTLs, on chromosomes 1, 2, 3, 4, 7, and 10 were found to come from the resistant parent Mo17. An additional QTL for resistance on chromosome 1 came from the susceptible parent B73. The eight identified QTLs accounted for 46% of the phenotypic variation for resistance. QTL × environment interactions often were highly significant but, with one exception, were the result of differences in the magnitude of QTL effects between years and not due to changes in direction of effects. QTLs on the long arm of chromosome 1 and chromosomes 2 and 3 had the largest effects, were the most consistently detected, and accounted for most of the phenotypic variance. No significant additive × additive epistatic effects were detected. These data support earlier reports of the polygenic inheritance of resistance to SLB of maize.

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