Genomic Architecture of Yield Performance of an Elite Rice Hybrid Revealed by its Derived Recombinant Inbred Line and Their Backcross Hybrid Populations

Background Since its development and wide adoption in China, hybrid rice has reached the yield plateau for more than three decades. To understand the genetic basis of heterosis in rice and accelerate hybrid rice breeding, the yield performances of the elite rice hybrid, Quan-you-si-miao (QYSM) were genetically dissected by whole-genome sequencing, large-scale phenotyping of 1061 recombined inbred lines (RILs) and 1061 backcross F 1 (BCF 1 ) hybrids derived from QYSM’s parents across three environments and gene-based analyses. Results Genome-wide scanning of 13,847 segregating genes between the parents and linkage mapping based on 855 bins across the rice genome and phenotyping experiments across three environments resulted in identification of large numbers of genes, 639 main-effect QTLs (M-QTLs) and 2736 epistatic QTLs with significant additive or heterotic effects on the trait performances of the combined population consisting of RILs and BCF 1 hybrids, most of which were environment-specific. The 324 M-QTLs affecting yield components included 32.7% additive QTLs, 38.0% over-dominant or dominant ones with strong and positive effects and 29.3% under-dominant or incomplete recessive ones with significant negative heterotic effects. 63.6% of 1403 genes with allelic introgression from subspecies japonica / Geng in the parents of QYSM may have contributed significantly to the enhanced yield performance of QYSM. Conclusions The parents of QYSM and related rice hybrids in China carry disproportionally more additive and under-dominant genes/QTLs affecting yield traits. Further focus in indica / Xian rice breeding should shift back to improving inbred varieties, while breaking yield ceiling of Xian hybrids can be achieved by one or combinations of the three strategies: (1) by pyramiding favorable alleles of additive genes, (2) by eliminating or minimizing under-dominant loci, and (3) by pyramiding overdominant/dominant genes polymorphic, particularly those underlying inter-subspecific heterosis.