Genome-wide association study and pathway analysis to decipher loci associated with Fusarium ear rot resistance in tropical maize germplasm.

Breeding for host resistance is the most efficient and environmentally safe method to curb the spread of fusarium ear rot (FER). However, conventional breeding for resistance to FER is hampered by the complex polygenic nature of this trait, which is highly influenced by environmental conditions. This study aimed to identify genomic regions, single nucleotide polymorphisms (SNPs), and putative candidate genes associated with FER resistance as well as candidate metabolic pathways and pathway genes involved in it. A panel of 151 tropical inbred maize lines were used to assess the genetic architecture of FER resistance over two seasons. During the study period, seven SNPs associated with FER resistance were identified on chromosomes 1, 2, 4, 5, and 9, accounting for 4-11% of the phenotypic variance. These significant markers were annotated into four genes. Seven significant metabolic pathways involved in FER resistance were identified using the Pathway Association Study Tool, the most significant being the superpathway of the glyoxylate cycle. Overall, this study confirmed that resistance to FER is indeed a complex mechanism controlled by several small to medium-effect loci. Our findings may contribute to fast-tracking the efforts to develop disease-resistant maize lines through marker-assisted selection. Supplementary Information: The online version contains supplementary material available at 10.1007/s10722-023-01793-4.

Genetic Variation Among Tropical Maize Inbred Lines from NARS and CGIAR Breeding Programs.

The use of molecular markers allows for precise estimates of genetic diversity, which is an important parameter that enables breeders to select parental lines and designing breeding systems. We assessed the level of genetic diversity and population structure in a panel of 151 tropical maize inbred lines using 10,940 SNP (single nucleotide polymorphism) markers generated through the DArTseq genotyping platform. The average gene diversity was 0.39 with expected heterozygosity ranging from 0.00 to 0.84, and a mean of 0.02. Analysis of molecular variance showed that 97% of allelic diversity was attributed to individual inbred lines within the populations while only 3% was distributed among the populations. Both neighbor-joining clustering and STRUCTURE analysis classified the inbred lines into four major groups. The crosses that involve inbred lines from most divergent subgroups are expected to generate maximum heterosis and produce wide variation. The results will be beneficial for breeders to better understand and exploit the genetic diversity available in the set of maize inbred lines we studied. Supplementary Information: The online version contains supplementary material available at 10.1007/s11105-022-01358-2.

Discovery of a major QTL for root-knot nematode (Meloidogyne incognita) resistance in cultivated sweetpotato (Ipomoea batatas).

KEY MESSAGE: Utilizing a high-density integrated genetic linkage map of hexaploid sweetpotato, we discovered a major dominant QTL for root-knot nematode (RKN) resistance and modeled its effects. This discovery is useful for development of a modern sweetpotato breeding program that utilizes marker-assisted selection and genomic selection approaches for faster genetic gain of RKN resistance. The root-knot nematode [Meloidogyne incognita (Kofoid & White) Chitwood] (RKN) causes significant storage root quality reduction and yields losses in cultivated sweetpotato [Ipomoea batatas (L.) Lam.]. In this study, resistance to RKN was examined in a mapping population consisting of 244 progenies derived from a cross (TB) between 'Tanzania,' a predominant African landrace cultivar with resistance to RKN, and 'Beauregard,' an RKN susceptible major cultivar in the USA. We performed quantitative trait loci (QTL) analysis using a random-effect QTL mapping model on the TB genetic map. An RKN bioassay incorporating potted cuttings of each genotype was conducted in the greenhouse and replicated five times over a period of 10 weeks. For each replication, each genotype was inoculated with ca. 20,000 RKN eggs, and root-knot galls were counted ~62 days after inoculation. Resistance to RKN in the progeny was highly skewed toward the resistant parent, exhibiting medium to high levels of resistance. We identified one major QTL on linkage group 7, dominant in nature, which explained 58.3% of the phenotypic variation in RKN counts. This work represents a significant step forward in our understanding of the genetic architecture of RKN resistance and sets the stage for future utilization of genomics-assisted breeding in sweetpotato breeding programs.