Identification of quantitative trait loci and the exploration of candidate genes for the tolerance to Zn deficiency in maize

Abstract Background Zn is essential for plants and Zn deficiency leads to great reduction in quality and quantity of crops. Maize, as one of the most important main staple crops worldwide, is more susceptible to Zn deficiency than any other cereal crops. Therefore, understanding the functional mechanisms in tolerance to Zn deficiency in maize is urgent but is still lacking. In this study, quantitative trait loci (QTL) analysis in K22 and By815 RIL population with high-density bin map was conducted to investigate genetic basis of the mechanisms in maize to tolerate Zn deficiency, subsequently some candidate genes were identified and considered as being associated with Zn metabolisms in plants. Results 21 QTLs were detected and accounted for 5.9% - 16.6% of phenotypic variations. Based on the co-localization in this study and the comparisons with previous studies in different RIL and GWAS populations, 223 candidate genes were identified inside the reduced QTL peak intervals on chromosome 1, 2, 6, 7 and 9. Furthermore, 9 genes detected within the peak bins of valuable genomic regions are suggested to be associated with ions transportation and some redox processes affected by Zn deficiency. Additionally, 5 genes, including ZmIRT1, ZmNRAMP6, ZmEIN2 and ZmHMAs, whose homologous gene have been studied and considered to be responsible for metal cations transportation and ethylene-signaling pathway requiring a transition metal were discovered in 5 loci we mapped. Conclusions 14 target genes identified in 9 loci we mapped in this work were explored to elucidate the potential functions in Zn homeostasis and the direct or indirect effects on mechanisms in Zn deficiency tolerance in maize. It is the first time that ZmIRT1, ZmNRAMP6, ZmHMAs were identified using linkage analysis under Zn deficiency in maize, providing genetic evidence and foundation for further gene functional characterization. Our findings have assisted us untangling the genetic basis of possible mechanisms in response to Zn deficiency in maize.