Aflatoxin contamination of maize grain is a huge economic and health problem, causing death and increased disease burden in much of the developing world and income loss in the developed world. Despite the gravity of the problem, deployable solutions are still being sought. In the past 15 years, much progress has been made in creating resistant maize inbred lines; mapping of genetic factors associated with resistance; and identifying possible resistance mechanisms. This review highlights this progress, most of which has occurred since the last time a review was published on this topic. Many of the needs highlighted in the last reviews have been addressed, and several solutions, taken together, can now greatly reduce the aflatoxin problem in maize grain. Continued research will soon lead to further solutions, which promise to further reduce and even eliminate the problem completely.

Background In maize hybrid breeding, complementary pools of parental lines with reshuffled genetic variants are established for superior hybrid performance. To comprehensively decipher the genetics of heterosis, we present a new design of multiple linked F1 populations with 42,840 F1 maize hybrids, generated by crossing a synthetic population of 1428 maternal lines with 30 elite testers from diverse genetic backgrounds and phenotyped for agronomic traits. Results We show that, although yield heterosis is correlated with the widespread, minor-effect epistatic QTLs, it may be resulted from a few major-effect additive and dominant QTLs in early developmental stages. Floral transition is probably one critical stage for heterosis formation, in which epistatic QTLs are activated by paternal contributions of alleles that counteract the recessive, deleterious maternal alleles. These deleterious alleles, while rare, epistatically repress other favorable QTLs. We demonstrate this with one example, showing that Brachytic2 represses the Ubiquitin3 locus in the maternal lines; in hybrids, the paternal allele alleviates this repression, which in turn recovers the height of the plant and enhances the weight of the ear. Finally, we propose a molecular design breeding by manipulating key genes underlying the transition from vegetative-to-reproductive growth. Conclusion The new population design is used to dissect the genetic basis of heterosis which accelerates maize molecular design breeding by diminishing deleterious epistatic interactions.

Plant phenotypic plasticity describes altered phenotypic performance of an individual when grown in different environments. Exploring genetic architecture underlying plant plasticity variation may help mitigate the detrimental effects of a rapidly changing climate on agriculture, but little research has been done in this area to date. In the present study, we established a population of 976 maize F1 hybrids by crossing 488 diverse inbred lines with two elite testers. Genome-wide association study (GWAS) identified hundreds of quantitative trait loci (QTLs) associated with phenotypic plasticity variation across diverse F1 hybrids, the majority of which contributed very little variance, in accordance with the polygenic nature of these traits. We identified several QTL regions that may have been selected during the tropical-temperate adaptation process. We also observed heterosis in terms of phenotypic plasticity, in addition to the traditional genetic value differences measured between hybrid and inbred lines, and the pattern of which was affected by genetic background. Our results demonstrate a landscape of phenotypic plasticity in maize, which will aid in the understanding of its genetic architecture, its contribution to adaptation and heterosis, and how it may be exploited for future maize breeding in a rapidly changing environment.