The resistance of tropical maize germplasm to ear rot caused by Fusarium verticillioides in Uganda

Abstract

Maize (Zea mays L.) is the third most important cereal in the world but unfortunately its yield is below what is expected and this could be attributed to various abiotic and biotic factors, one of them being Fusarium ear rot. Global maize production is impacted by the destructive fungal disease known as Fusarium ear rot, which is caused by Fusarium verticillioides. In addition to causing significant yield losses, it also produces toxic mycotoxins such as Fumonisins which are harmful to both humans and livestock if consumed. The occurrence of ear rots can vary greatly from year to year as well as field to field. This disease causes great concern in maize production worldwide, as it is considered to have a severe impact on the maize grain yield and income in the market. The best approach to manage Fusarium ear rot (FER) is to breed for resistance since there are no documented FER resistant varieties in Uganda. This study set out to: i) identify possible sources of Fusarium ear rot resistance, ii) evaluate the type of gene action governing FER resistance, and iii) pinpoint genomic regions and putative genes associated with FER resistance in maize. In the first part of the study, a genetically diverse collection of 150 maize inbred lines was screened as probable sources of resistance to FER using artificial inoculation with the toothpick method in the field for two seasons. At harvest, ears were scored for FER severity and scored. Significant differences were noted between the two seasons, with inbred lines exhibiting varied levels of performance. Ten inbred lines consistently exhibited low disease severity across both seasons, suggesting they could serve as valuable sources of resistance for breeding programs. The second study investigated the gene action behind resistance to infection by F. verticillioides in 13 inbred lines. The North Carolina II mating design was used to generate 42 hybrids which were then evaluated in five environments. The Genotype X environment interaction was highly significant (P < 0.001), as well the GCA effects and the GCA X environment interactions. Inbred lines JPS31-89, JPS31-167, JPS30-5, JPS30-9 and JPS30-11 emerged as the best combiners for FER making them good candidates to use in breeding resistant varieties. Additive gene effects played a more significant role than non-additive gene effects in conferring resistance to FER. The hybrids JPS30-11/JPS30-13, JPS30-12/JPS30-21, and JPS30-11/JPS31-4 were identified as the most effective combinations for FER resistance. Using DarTseq markers, the final study sought to identify genomic regions and potential genes associated with FER resistance. A total of 20,900 single nucleotide polymorphisms (SNPs) were used to genotype 150 inbred lines. Two significant SNP markers on chromosomes 1, and 4 were found by the Genome-Wide Association Study (GWAS) and these accounted for 9.8 and 11.9% of the phenotypic variation. The significant SNP marker 2396181|F|0-39:G>T-39:G>T identified on chromosome 1 was annotated to the candidate gene GRMZM2G104516, which encodes zinc finger proteins. These proteins play critical roles in various biological processes, including transcription, DNA recognition, translation, RNA packaging, photosynthesis, and regulating resistance mechanisms to both biotic (pathogen response) and abiotic stresses. On chromosome 4, SNP marker 2463074|F|0-20:G>A-20:G>A was annotated to candidate gene was GRMZM2G047319 which belongs to the serine/threonine protein class which play a role in signalling during pathogen recognition and the subsequent activation of plant defence responses. These results showed that resistance to FER is a complex trait regulated by several genes with small effects, and it involves multiple pathways. More in-depth biochemical and molecular studies are recommended to understand this trait as well as validate these markers to be used for breeding for resistance to Fusarium ear rot.