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Key message A key genomic region was identified for resistance to FSR at 168 Mb on chromosome 6 in GWAS and haplotype regression analysis, which was validated by QTL mapping in two populations. Abstract Fusarium stalk rot (FSR) of maize is an economically important post-flowering stalk rot (PFSR) disease caused by Fusarium verticillioides. The pathogen invades the plant individually, or in combination with other stalk rot pathogens or secondary colonizers, thereby making it difficult to make accurate selection for resistance. For identification and validation of genomic regions associated with FSR resistance, a genome-wide association study (GWAS) was conducted with 342 maize lines. The panel was screened for FSR in three environments using standard artificial inoculation methodology. GWAS using the mixed linear model corrected for population structure and kinship was done, in which 290,626 SNPs from genotyping-by-sequencing were used. A total of 7 SNPs, five on chromosome 6 showing strong LD at 168 Mb, were identified to be associated with FSR. Haplotype regression analysis identified 32 haplotypes with a significant effect on the trait. In a QTL mapping experiment in two populations for validating the identified variants, QTLs were identified with confidence intervals having overlapped physical coordinates in both the populations on chromosome 6, which was closely located to the GWAS-identified variants on chromosome 6. It makes this genomic region a crucial one to further investigate the possibility of developing trait markers for deployment in breeding pipelines. It was noted that previously reported QTLs for other stalk rots in maize mapped within the same physical intervals of several haplotypes identified for FSR resistance in this study. The possibility of QTLs controlling broad-spectrum resistance for PFSR in general requires further investigation.
Key message A key genomic region was identified for resistance to FSR at 168 Mb on chromosome 6 in GWAS and haplotype regression analysis, which was validated by QTL mapping in two populations. Abstract Fusarium stalk rot (FSR) of maize is an economically important post-flowering stalk rot (PFSR) disease caused by Fusarium verticillioides. The pathogen invades the plant individually, or in combination with other stalk rot pathogens or secondary colonizers, thereby making it difficult to make accurate selection for resistance. For identification and validation of genomic regions associated with FSR resistance, a genome-wide association study (GWAS) was conducted with 342 maize lines. The panel was screened for FSR in three environments using standard artificial inoculation methodology. GWAS using the mixed linear model corrected for population structure and kinship was done, in which 290,626 SNPs from genotyping-by-sequencing were used. A total of 7 SNPs, five on chromosome 6 showing strong LD at 168 Mb, were identified to be associated with FSR. Haplotype regression analysis identified 32 haplotypes with a significant effect on the trait. In a QTL mapping experiment in two populations for validating the identified variants, QTLs were identified with confidence intervals having overlapped physical coordinates in both the populations on chromosome 6, which was closely located to the GWAS-identified variants on chromosome 6. It makes this genomic region a crucial one to further investigate the possibility of developing trait markers for deployment in breeding pipelines. It was noted that previously reported QTLs for other stalk rots in maize mapped within the same physical intervals of several haplotypes identified for FSR resistance in this study. The possibility of QTLs controlling broad-spectrum resistance for PFSR in general requires further investigation.
Fusarium stalk rot (FSR) is a global destructive disease in maize, the e ciency of phenotypic selection for improving FSR resistance was low. Novel genomic tools -genome-wide association study (GWAS) and genomic prediction (GP) -provide an opportunity for genetic dissection and improving FSR resistance. In this study, GWAS and GP analyses were performed on 562 tropical maize inbred lines consisting of two populations in four environments under arti cial inoculation. In total, 15 SNPs signi cantly associated with FSR resistance were identi ed across two populations and the CombinedPOP consisting of all 562 inbred lines, with the P-values ranging from 1.99×10 -7 to 8.27×10 -13 , and the phenotype variance explained (PVE) values ranging from 0.94 to 8.30%. The effects of the 15 favorable alleles ranged from -4.29 to -14.21%. One stable genomic region in the interval of 0.95 Mb from 250,089,724 bp to 251,044,933 bp on chromosome 1 was detected across all populations, and the PVE values of the detected SNPs ranged from 2.16 to 5.18%. Medium GP accuracy of FSR severity, 0.29 to 0.51, was observed in two cross-validation (CV) schemes. When incorporating genotype-by-environment interaction, GP accuracy was improved from 0.36 to 0.40 in the CV1 scheme, and from 0.42 to 0.55 in the CV2 scheme. Considering both the genome coverage and the total PVE of SNPs for selecting a subset of molecular markers further improved the GP accuracy. These ndings extend the knowledge of exploiting genomic tools for genetic dissection and improving FSR resistance in tropical maize. Key MessageA stable genomic region conferring FSR resistance at ~250 Mb on chromosome 1 was identi ed by GWAS. The potential of genomic prediction was proved in FSR resistance breeding.
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