Fine mapping and candidate gene prediction of a major quantitative trait locus for tassel branch number in maize

Tassel branch number (TBN) is the principal component of tassel inflorescence architecture in the maize plant. TBN is believed to be controlled by a set of quantitative trait loci (QTLs). However, it is necessary to identify and genetically evaluate these QTLs before the TBN can be improved upon using a molecular breeding approach. Therefore, in this study, we developed the chromosome segment introgression line (CSIL) TBN1 with the Zong31 (Z31) background and a higher TBN, and then we utilized the CSIL-TBN1-derived populations and identified a major QTL, qTBN6a, by linkage analysis. Fine mapping of the qTBN6a QTL was validated using a set of sub-CSILs and located in a 240-kb genomic region (Bin6.07) in B73RefGen_v4. One allele included in the introgression fragment had a positive effect, noticeably increasing the TBN and demonstrating the potential to improve the TBN of Z31. Afterward, in the qTBN6a interval, gene expression, sequence alignment, functional analysis, and the analysis of motifs in the 5' UTR suggested that candidate genes of qTBN6a are important functional genes at the early stage of immature infected tassel development. Among these candidate genes, a long W22::Mu-insertion/deletion in exon one and an 11-bp insertion/deletion in the promoter region may affect the variation of the qTBN6a QTL observed between Z31 and TBN1. In addition, the candidate genes of qTBN6a were found to encode a pentatricopeptide repeat (PPR)-containing protein and a histone deacetylase (HDA), which are known to be closely associated with RNA editing and stability and chromatin state activity for the transcription of gene expression, respectively. Finally, a model of qTBN6a based on the synergistic regulation of PPR and HDA for the maintenance of inflorescence meristem (IM) identity and its differentiation to the branch meristem (BM) in TBN1 was suggested. Collectively, our results provide an available locus for the molecular improvement of TBN and the isolation of functional genes underlying this QTL.