Effects of the quantitative trait locus qPss3 on inhibition of photoperiod sensitivity and resistance to stalk rot disease in maize.

KEY MESSAGE: We identified a quantitative trait locus, qPss3, and fine-mapped the causal locus to a 120-kb interval in maize. This locus inhibits the photoperiod sensitivity caused by ZmCCT9 and ZmCCT10, resulting in earlier flowering by 2 ~ 4 days without reduction in stalk-rot resistance in certain genotypes. Photoperiod sensitivity is a key factor affecting the adaptation of maize (Zea mays L.) to high-latitude growing areas. Although many genes associated with flowering time have been identified in maize, no gene that inhibits photoperiod sensitivity has been reported. In our previous study, we detected large differences in photoperiod sensitivity among maize inbred lines with the same photoperiod-sensitive allele at the ZmCCT10 locus. Here, we used two segregating populations with the same genetic backgrounds but different ZmCCT10 alleles to perform quantitative trait locus (QTL) analysis. We identified a unique QTL, qPss3, on chromosome 3 in the population carrying the sensitive ZmCCT10 allele. After sequential fine-mapping, we eventually delimited qPss3 to an interval of ~ 120 kb. qPss3 behaved as a dominant locus and caused earlier flowering by 2-4 days via inhibiting ZmCCT10-induced photoperiod sensitivity under long-day conditions. qPss3 also inhibited the photoperiod sensitivity induced by another flowering-related gene, ZmCCT9. For application in agriculture, an F1 hybrid heterozygous at both qPss3 and ZmCCT10 loci constitutes an optimal allele combination, showing high resistance to stalk rot without a significant delay in flowering time. Moreover, qPss3 is of great value in regulating the flowering time of tropical maize grown at high-latitude regions.

Combined genome-wide association study and transcriptome analysis reveal candidate genes for resistance to Fusarium ear rot in maize.

Fusarium ear rot, caused by Fusarium verticillioides, is a devastating fungal disease in maize that reduces yield and quality; moreover, F. verticillioides produces fumonisin mycotoxins, which pose serious threats to human and animal health. Here, we performed a genome-wide association study (GWAS) under three environmental conditions and identified 34 single-nucleotide polymorphisms (SNPs) that were significantly associated with Fusarium ear rot resistance. With reference to the maize B73 genome, 69 genes that overlapped with or were adjacent to the significant SNPs were identified as potential resistance genes to Fusarium ear rot. Comparing transcriptomes of the most resistant and most susceptible lines during the very early response to Fusarium ear rot, we detected many differentially expressed genes enriched for pathways related to plant immune responses, such as plant hormone signal transduction, phenylpropanoid biosynthesis, and cytochrome P450 metabolism. More than one-fourth of the potential resistance genes detected in the GWAS were differentially expressed in the transcriptome analysis, which allowed us to predict numbers of candidate genes for maize resistance to ear rot, including genes related to plant hormones, a MAP kinase, a PR5-like receptor kinase, and heat shock proteins. We propose that maize plants initiate early immune responses to Fusarium ear rot mainly by regulating the growth-defense balance and promoting biosynthesis of defense compounds.

qRfg3, a novel quantitative resistance locus against Gibberella stalk rot in maize.

KEY MESSAGE: A quantitative trait locus  qRfg3 imparts recessive resistance to maize Gibberella stalk rot. qRfg3 has been mapped into a 350-kb interval and could reduce the disease severity index by ~26.6%. Gibberella stalk rot, caused by the fungal pathogen Fusarium graminearum, severely affects maize yield and grain quality worldwide. To identify more resistance quantitative trait loci (QTLs) against this disease, we analyzed a recombinant inbred line (RIL) population derived from a cross between resistant H127R and susceptible C7-2 inbred lines. Within this population, maize resistance to Gibberella stalk rot had high broad-sense heritability. A major QTL, qRfg3, on chromosome 3 was consistently detected across three field trials, accounting for 10.7-19.4% of the total phenotypic variation. Using a progeny-based sequential fine-mapping strategy, we narrowed qRfg3 down to an interval of ~350 kb. We further demonstrated that qRfg3 is a recessive resistance locus to Gibberella stalk rot that reduced the disease severity index by ~26.6%. Both the gene location and recessive genetic mode distinguish qRfg3 from other stalk rot resistance loci. Hence, qRfg3 is valuable as a complement to existing resistance QTLs to improve maize resistance to Gibberella stalk rot.