scholarly journals Co-inoculation of aflatoxigenic and non-aflatoxigenic strains of Aspergillus flavus to study fungal invasion, colonization, and competition in maize kernels

2014 ◽  
Vol 5 ◽  
Author(s):  
Zuzana Hruska ◽  
Kanniah Rajasekaran ◽  
Haibo Yao ◽  
Russell Kincaid ◽  
Dawn Darlington ◽  
...  
2008 ◽  
Vol 165 (2) ◽  
pp. 89-97 ◽  
Author(s):  
Kanniah Rajasekaran ◽  
Jeffrey W. Cary ◽  
Peter J. Cotty ◽  
Thomas E. Cleveland

2014 ◽  
Vol 5 ◽  
Author(s):  
Andrea L. Dolezal ◽  
Xiaomei Shu ◽  
Gregory R. OBrian ◽  
Dahlia M. Nielsen ◽  
Charles P. Woloshuk ◽  
...  

1993 ◽  
Vol 56 (11) ◽  
pp. 967-971 ◽  
Author(s):  
ROBERT L. BROWN ◽  
PETER J. COTTY ◽  
THOMAS E. CLEVELAND ◽  
NEIL W. WIDSTROM

Kernels from two maize populations, MAS:gk and MAS:pw,nf, showed significant postharvest resistance to aflatoxin contamination by Aspergillus flavus but showed no significant inter-population variation for this resistance. Growth of A. flavus on both populations was significantly less than on susceptible control lines. Kernels from the resistant populations retained resistance when wounded through the pericarp prior to inoculation with A. flavus, despite the fact that the exposed endosperm supported good fungal growth. Kernels from these populations also retained resistance when they were acetone washed before inoculation. Resistance to aflatoxin contamination was lost in kernels that were autoclaved, crushed, or embryo wounded. All assays were incubated under conditions favorable to kernel germination. Results suggest that postharvest resistance to aflatoxin contamination in these two populations is related to metabolic activities of the living com embryo.


2013 ◽  
Vol 162 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Antonio Mauro ◽  
Paola Battilani ◽  
Kenneth A. Callicott ◽  
Paola Giorni ◽  
Amedeo Pietri ◽  
...  

1997 ◽  
Vol 87 (2) ◽  
pp. 164-169 ◽  
Author(s):  
C. P. Woloshuk ◽  
J. R. Cavaletto ◽  
T. E. Cleveland

Aflatoxin biosynthesis was induced by compounds in filtrates (EF) obtained from cultures consisting of ground maize kernels colonized by Aspergillus flavus. The inducing activity increased to a maximum at 4 days of incubation and then decreased. Amylase activity was detected in the EF, suggesting that the inducers are products of starch degradation (glucose, maltose, and maltotriose). Analysis of the enzyme by isoelectric focusing electrophoresis indicated a single α-amylase with a pI of 4.3. No maltase or amyloglucosidase was detected in the EF. High-pressure liquid chromatography analysis of the EF indicated the presence of glucose, maltose, and maltotriose in near-equal molar concentrations (about 15 mM). With a β-glucuronidase (GUS) reporter assay consisting of A. flavus transformed with an aflatoxin gene promoter-GUS reporter gene fusion to monitor induction of aflatoxin biosynthesis, the minimum concentration of glucose, maltose, or maltotriose that induced measurable GUS activity was determined to be 1 mM. These results support the hypothesis that the best inducers of aflatoxin biosynthesis are carbon sources readily metabolized via glycolysis. They also suggest that α-amylase produced by A. flavus has a role in the induction of aflatoxin biosynthesis in infected maize kernels.


1999 ◽  
Vol 89 (10) ◽  
pp. 908-914 ◽  
Author(s):  
A. M. Fakhoury ◽  
C. P. Woloshuk

Aspergillus flavus is the causal agent of an ear and kernel rot in maize. In this study, we characterized an α-amylase-deficient mutant and assessed its ability to infect and produce aflatoxin in wounded maize kernels. The α-amylase gene Amy1 was isolated from A. flavus, and its DNA sequence was determined to be nearly identical to Amy3 of A. oryzae. When Amy1 was disrupted in an aflatoxigenic strain of A. flavus, the mutant failed to produce extracellular α-amylase and grew 45% the rate of the wild-type strain on starch medium. The mutant produced aflatoxin in medium containing glucose but not in a medium containing starch. The α-amylase-deficient mutant produced aflatoxin in maize kernels with wounded embryos and occasionally produced aflatoxin only in embryos of kernels with wounded endosperm. The mutant strain failed to produce aflatoxin when inoculated onto degermed kernels. In contrast, the wild-type strain produced aflatoxin in both the endosperm and embryo. These results suggest that α-amylase facilitates aflatoxin production and growth of A. flavus from a wound in the endosperm to the embryo. A 14-kDa trypsin inhibitor associated with resistance to A. flavus and aflatoxin in maize also inhibited the α-amylase from A. flavus, indicating that it is a bifunctional inhibitor. The inhibitor may have a role in resistance, limiting the growth of the fungus in the endosperm tissue by inhibiting the degradation of starch.


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