Abstract

The QTL hotspots determining seed glucosinolate content instead of only four HAG1 loci and elucidation of a potential regulatory model for rapeseed SGC variation. Glucosinolates (GSLs) are amino acid-derived, sulfur-rich secondary metabolites that function as biopesticides and flavor compounds, but the high seed glucosinolate content (SGC) reduces seed quality for rapeseed meal. To dissect the genetic mechanism and further reduce SGC in rapeseed, QTL mapping was performed using an updated high-density genetic map based on a doubled haploid (DH) population derived from two parents that showed significant differences in SGC. In 15 environments, a total of 162 significant QTLs were identified for SGC and then integrated into 59 consensus QTLs, of which 32 were novel QTLs. Four QTL hotspot regions (QTL-HRs) for SGC variation were discovered on chromosomes A09, C02, C07 and C09, including seven major QTLs that have previously been reported and four novel major QTLs in addition to HAG1 loci. SGC was largely determined by superimposition of advantage allele in the four QTL-HRs. Important candidate genes directly related to GSL pathways were identified underlying the four QTL-HRs, including BnaC09.MYB28, BnaA09.APK1, BnaC09.SUR1 and BnaC02.GTR2a. Related differentially expressed candidates identified in the minor but environment stable QTLs indicated that sulfur assimilation plays an important rather than dominant role in SGC variation. A potential regulatory model for rapeseed SGC variation constructed by combining candidate GSL gene identification and differentially expressed gene analysis based on RNA-seq contributed to a better understanding of the GSL accumulation mechanism. This study provides insights to further understand the genetic regulatory mechanism of GSLs, as well as the potential loci and a new route to further diminish the SGC in rapeseed.

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