Literature DB >> 27709251

Low validation rate of quantitative trait loci for Gibberella ear rot resistance in European maize.

Pedro Correa Brauner1, Albrecht E Melchinger1, Tobias A Schrag1, H Friedrich Utz1, Wolfgang Schipprack1, Bettina Kessel2, Milena Ouzunova2, Thomas Miedaner3.   

Abstract

KEY MESSAGE: Six quantitative trait loci (QTL) for Gibberella ear rot resistance in maize were tested in two different genetic backgrounds; three QTL displayed an effect in few near isogenic line pairs. Few quantitative trait loci (QTL) mapping studies for Gibberella ear rot (GER) have been conducted, but no QTL have been verified so far. QTL validation is prudent before their implementation into marker-assisted selection (MAS) programs. Our objectives were to (1) validate six QTL for GER resistance, (2) evaluate the QTL across two genetic backgrounds, (3) investigate the genetic background outside the targeted introgressions. Pairs of near isogenic lines (NILs) segregating for a single QTL (Qger1, Qger2, Qger10, Qger13, Qger16, or Qger21) were developed by recurrent backcross until generation BC3S2. Donor parents (DP) carrying QTL were backcrossed to a susceptible (UH009) and a moderately resistant (UH007) recurrent parent. MAS was performed using five SNP markers covering a region of 40 cM around each QTL. All NILs were genotyped with the MaizeSNP50 assay and phenotyped for GER severity and deoxynivalenol and zearalenone content. Traits were significantly (P < 0.001) intercorrelated. Out of 34 NIL pairs with the UH009 genetic background, three pairs showed significant differences in at least one trait for three QTL (Qger1, Qger2, Qger13). Out of 25 NIL pairs with the UH007 genetic background, five pairs showed significant differences in at least one trait for two QTL (Qger2, Qger21). However, Qger16, Qger10 and Qger13 were most likely false positives. The genetic background possibly affected NIL pairs comparisons due to linkage drag and/or epistasis with residual loci from the DP in non-target regions. In conclusion, validation rates were disappointingly low, which further indicates that GER resistance is controlled by many low-effect QTL.

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Year:  2016        PMID: 27709251     DOI: 10.1007/s00122-016-2802-3

Source DB:  PubMed          Journal:  Theor Appl Genet        ISSN: 0040-5752            Impact factor:   5.699


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