Role of Calcineurin Gene and Antimicrobial Compounds in Conidiation of Aspergillus flavus

Abstract

Aspergillus flavus is a facultative, plant parasitic pathogen, with the ability to infect several common crop species including corn, cotton, peanuts, and many other crops (Fountain et al., 2014). Economic losses due to the infection of grain crops such as maize by A. flavus is not only due to the expression of symptoms known as Aspergillus ear rot but also due to the subsequent contamination of the grain with mycotoxins called aflatoxin. Although Link first described this species in 1809, biology and pathogenicity of A. flavus was not studied extensively until the mid-1960s when the incidence of Turkey X disease which killed over 100,000 turkey poults due to aflatoxin contaminated feed associated with A. flavus infected peanuts. This resulted in broad screening of feed and food. Chemical structures of the major aflatoxins were elucidated, and research was conducted to prevent post-harvest contamination of grain crops through the modulation of storage conditions. However, during a particularly severe outbreak of aflatoxin contamination in maize in the late 1970s in the U.S. it was found that A. flavus could both, colonize and produce aflatoxin on developing maize kernels prior to harvest. (Fountain et al., 2014) Since then, research efforts have been focused on determining the source of host plant resistance to prevent A. flavus infection and subsequent aflatoxin production pre-harvest and before transportation to storage. Numerous techniques and approaches have been employed including modern plant breeding and genetics tools such as proteomic, transcriptomic, and biochemical analyses in order to discover the mechanism responsible for host plant resistance and the interaction between the two organisms (Fountain et al., 2014). Till date, it has been established that resistance is inherited quantitatively with a strong genotype by environmental influence (Fountain et al., 2014). It is a complex interaction with a high environmentally induced variability and abiotic and biotic stress strongly influencing resistance or susceptibility.