Plant height (PH) and ear height (EH) are two very important agronomic traits related to the population density and lodging in maize. In order to better understand of the genetic basis of nature variation in PH and EH, two bi-parental populations and one genome-wide association study (GWAS) population were used to map quantitative trait loci (QTL) for both traits. Phenotypic data analysis revealed a wide normal distribution and high heritability for PH and EH in the three populations, which indicated that maize height is a highly polygenic trait. A total of 21 QTL for PH and EH in three common genomic regions (bin 1.05, 5.04/05, and 6.04/05) were identified by QTL mapping in the two bi-parental populations under multiple environments. Additionally, 41 single nucleotide polymorphisms (SNPs) were identified for PH and EH by GWAS, of which 29 SNPs were located in 19 unique candidate gene regions. Most of the candidate genes were related to plant growth and development. One QTL on Chromosome 1 was further verified in a near-isogenic line (NIL) population, and GWAS identified a C2H2 zinc finger family protein that maybe the candidate gene for this QTL. These results revealed that nature variation of PH and EH are strongly controlled by multiple genes with low effect and facilitated a better understanding of the underlying mechanism of height in maize.

Fusarium verticillioides is the most commonly reported fungal species responsible for ear rot of maize which substantially reduces grain yield. It also results in a substantial accumulation of mycotoxins that give rise to toxic response when ingested by animals and humans. For inefficient control by chemical and agronomic measures, it thus becomes more desirable to select more resistant varieties. However, the molecular mechanisms underlying the infection process remain poorly understood, which hampers the application of quantitative resistance in breeding programs. Here, we reveal the disease-resistance mechanism of the maize inbred line of BT-1 which displays high resistance to ear rot using RNA high throughput sequencing. By analyzing RNA-seq data from the BT-1 kernels before and after F. verticillioides inoculation, we found that transcript levels of genes associated with key pathways are dramatically changed compared with the control treatment. Differential gene expression in ear rot resistant and susceptible maize was confirmed by RNA microarray and qRT-PCR analyses. Further investigation suggests that the small heat shock protein family, some secondary metabolites, and the signaling pathways of abscisic acid, jasmonic acid, or salicylic acids (SA) may be involved in the pathogen-associated molecular pattern-triggered immunity against F. verticillioides. These data will not only provide new insights into the molecular resistant mechanisms against fungi invading, but may also result in the identification of key molecular factors associated with ear rot resistance in maize.

Fusarium verticillioides can be transmitted via seeds and cause systemic infection in maize (Zea mays L.); its mycotoxin has harmful effects on animal and human health. We combined QTL mapping in recombinant inbred line (RIL) populations with a genome-wide association study (GWAS) of 217 diverse maize lines using 224,152 single nucleotide polymorphisms (SNPs) under controlled conditions to determine the genetic architecture of F. verticillioides seed rot (FSR) resistance. Our study identified 8 quantitative trait loci (QTLs) and 43 genes associated with 57 SNPs that were correlated with FSR resistance through linkage mapping and GWAS, respectively. Among these, there were three candidate genes, namely GRMZM2G0081223, AC213654.3_FG004, and GRMZM2G099255, which were detected in both linkage mapping and GWAS. Furthermore, the near-isogenic lines (NILs) containing GRMZM2G0081223, which also had a susceptible parent background, were found to have a significantly improved level of resistance. In addition, the expression profile of the three candidate genes revealed that they all respond to the infection following inoculation with F. verticillioides. These genetic analyses indicate that FSR resistance is controlled by loci with minor effect, and the polymerization breeding of lines with beneficial alleles and candidate genes could improve FSR resistance in maize.Maize is one of the most important cereals in the world due to its high yield potential and its high demand for use as food, feed, and for industrial purposes. Maize is subject to a variety of biotic and abiotic stresses during its lifetime, which can significantly affect final yield and quality. The planting area for maize in China is 37.07 million hectares, of which the Huang-Huai-Hai region accounts for 39%. In this region, the incidence of soil-borne diseases in maize has increased over the years, which coincides with increases in the use of cultivation systems such as double cropping, no-tillage, and straw returned. Fusarium verticillioides (formerly Fusarium moniliforme), which is a commonly-found soil-borne fungal species, can be transmitted to seeds and cause systemic infection in maize 1 . Previous studies have confirmed that seeds infected with F. verticillioides are a source of root and stalk infection 2 . In addition, the fungus can be transmitted from the planted seed through to the developing kernels via the mature plant 1,[3][4][5] . The diseases caused by F. verticillioides include seedling blight, stalk rot, root rot, kernel rot, ear rot, and seed rot 5,6 . F. verticillioides infection can result in decreased grain yields, poor grain quality, and contamination by the mycotoxin fumonisin 7 . The fumonisins produced by F. verticillioides are known to cause a variety of diseases when ingested by animals, and have been implicated in human carcinogenesis and neural tube defects, as well as in plant diseases 6 .

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Background: Fusarium ear rot (FER) caused by Fusarium verticillioides is a major disease of maize that reduces grain yield and quality globally. However, there have been few reports of major loci for FER were verified and cloned. Result: To gain a comprehensive understanding of the genetic basis of natural variation in FER resistance, a recombinant inbred lines (RIL) population and one panel of inbred lines were used to map quantitative trait loci (QTL) for resistance. As a result, a total of 10 QTL were identified by linkage mapping under four environments, which were located on six chromosomes and explained 1.0-7.1% of the phenotypic variation. Epistatic mapping detected four pairs of QTL that showed significant epistasis effects, explaining 2.1-3.0% of the phenotypic variation. Additionally, 18 single nucleotide polymorphisms (SNPs) were identified across the whole genome by genomewide association study (GWAS) under five environments. Compared linkage and association mapping revealed five common intervals located on chromosomes 3, 4, and 5 associated with FER resistance, four of which were verified in different near-isogenic lines (NILs) populations. GWAS identified three candidate genes in these consistent intervals, which belonged to the Glutaredoxin protein family, actin-depolymerizing factors (ADFs), and AMP-binding proteins. In addition, two verified FER QTL regions were found consistent with Fusarium cob rot (FCR) and Fusarium seed rot (FSR). Conclusions: These results revealed that multi pathways were involved in FER resistance, which was a complex trait that was controlled by multiple genes with minor effects, and provided important QTL and genes, which could be used in molecular breeding for resistance.