Abstract

Tar spot complex (TSC) is one of the most important foliar diseases in tropical maize. TSC resistance could be furtherly improved by implementing marker-assisted selection (MAS) and genomic selection (GS) individually, or by implementing them stepwise. Implementation of GS requires a profound understanding of factors affecting genomic prediction accuracy. In the present study, an association-mapping panel and three doubled haploid populations, genotyped with genotyping-by-sequencing, were used to estimate the effectiveness of GS for improving TSC resistance. When the training and prediction sets were independent, moderate-to-high prediction accuracies were achieved across populations by using the training sets with broader genetic diversity, or in pairwise populations having closer genetic relationships. A collection of inbred lines with broader genetic diversity could be used as a permanent training set for TSC improvement, which can be updated by adding more phenotyped lines having closer genetic relationships with the prediction set. The prediction accuracies estimated with a few significantly associated SNPs were moderate-to-high, and continuously increased as more significantly associated SNPs were included. It confirmed that TSC resistance could be furtherly improved by implementing GS for selecting multiple stable genomic regions simultaneously, or by implementing MAS and GS stepwise. The factors of marker density, marker quality, and heterozygosity rate of samples had minor effects on the estimation of the genomic prediction accuracy. The training set size, the genetic relationship between training and prediction sets, phenotypic and genotypic diversity of the training sets, and incorporating known trait-marker associations played more important roles in improving prediction accuracy. The result of the present study provides insight into less complex trait improvement via GS in maize.

Highlights

  • Tar spot complex (TSC), caused by an interaction of at least three fungal species: Phyllachora maydis; Monographella maydis; and Coniothyrium phyllachorae, is one of the most important foliar diseases of maize (Zea mays L. subsp. mays) in many Central and South American tropical and subtropical areas (Hock et al, 1992; Pereyda-Hernández et al, 2009)

  • The genetic architecture of TSC resistance in maize was confirmed by combined association mapping (AM) and linkage mapping using higher marker density, the major quantitative resistance locus (QTL) on bin 8.03 was narrowed down to a 33.6 million base pair region, and the results showed that TSC resistance in maize is controlled by a major QTL on bin 8.03, coupled with several minor QTL with smaller effects on other chromosomes (Cao et al, 2017)

  • A few genetic studies have been conducted to dissect the genetic architecture of resistance to TSC of maize (Mahuku et al, 2016; Cao et al, 2017), where the heritabilities of TSC in different populations were medium-to-high, revealing that the phenotypic selection is effective for improving TSC resistance

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Summary

Introduction

Tar spot complex (TSC), caused by an interaction of at least three fungal species: Phyllachora maydis; Monographella maydis; and Coniothyrium phyllachorae, is one of the most important foliar diseases of maize (Zea mays L. subsp. mays) in many Central and South American tropical and subtropical areas (Hock et al, 1992; Pereyda-Hernández et al, 2009). Development and deployment of maize varieties with genetic resistance is the most economical and effective strategy for controlling TSC (Ceballos and Deutsch, 1992). A few studies have been conducted to dissect the genetic architecture of TSC resistance in maize (Mahuku et al, 2016; Cao et al, 2017). The genetic architecture of TSC resistance in maize was confirmed by combined AM and linkage mapping using higher marker density, the major QTL on bin 8.03 was narrowed down to a 33.6 million base pair region, and the results showed that TSC resistance in maize is controlled by a major QTL on bin 8.03, coupled with several minor QTL with smaller effects on other chromosomes (Cao et al, 2017)

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