Genetic basis of heterosis for yield and yield components explored by QTL mapping across four genetic populations in upland cotton

Abstract

Background: Quantitative trait loci (QTL) mapping provides a powerful tool to unravel the genetic bases of cotton yield and its components, as well as their heterosis. In the present study, the genetic basis underlying inbreeding depression and heterosis for yield and yield components of upland cotton was investigated in recombinant inbred line (RIL), immortalized F₂ (IF₂), and two backcross (BCF₁) populations based on a high-density SNP linkage map across four environments.

Results: Significant inbreeding depression of fruit branches per plant (FB), boll numbers per plant (BN), seed cotton yield (SY), and lint yield (LY) in RIL population and high levels of heterosis for SY, LY, and boll weight (BW) in IF₂ and two BCF₁ populations were observed. A total of 285 QTLs were identified in the four related populations using a composite interval mapping approach. In the IF₂ population, 26.60% partially dominant (PD) QTLs and 71.28% over-dominant (OD) QTLs were identified. In two BCF₁ populations, 42.41% additive QTLs, 4.19% PD QTLs, and 53.40% OD QTLs were detected. For multi-environment analysis, phenotypic variances (PV) explained by e-QTLs were higher than those by m-QTLs in each of the populations, and the average PV of m-QTLs and e-QTLs explained by QTL × environment interactions occupied a considerable proportion of total PV in all seven datasets.

Conclusions: At the single-locus level, the genetic bases of heterosis varied in different populations. Partial dominance and over-dominance were the main cause of heterosis in the IF₂ population, while additive effects and over-dominance were the main genetic bases of heterosis in two BCF₁ populations. In addition, the various genetic components to heterosis presented trait specificity. In the multi-environment model analysis, epistasis was a common feature of most loci associated with inbreeding depression and heterosis. Furthermore, the environment was a critical factor in the expression of these m-QTLs and e-QTLs. Altogether, additive effects, over-dominance, epistasis and environmental interactions all contributed to the heterosis of yield and its components in upland cotton, with over-dominance and epistasis more important than the others.

Keywords: Backcross population; Epistasis; Hybrid; Immortalized F2 population; Inbreeding depression; Over-dominance.

Fig. 1

Diagram of the development scheme for the RIL, IF₂, and two BCF_I populations. a Crosses were made between two different lines from RIL_A and RIL_B (for example, RIL_A1 × RIL_B2). Here, RIL_A and RIL_B represent female and male RIL lines, respectively. This procedure was repeated two times, and finally 376 lines were produced, forming the IF₂ population. The IF₂MPH dataset derived from the IF₂ population included 376 mid-parental heterosis (MPH) values (H), which were estimated by MPH = F₁ – MP (Hua et al. 2003). Here, F₁ represents the observations in the IF₂ populations, and MP represents the average trait value between their parents. b, c The HSBCF₁ and MARBCF₁ populations were produced by RILs × P₁ and RILs × P₂, respectively, and each contained 188 lines. The RILs were used as the female parents in two backcross designs with the two original parents. The HSBCF₁MPH and MARBCF₁MPH datasets also each included 188 individuals (H) and were estimated by MPH = F₁ – MP (Hua et al. 2003). Here, F₁ represents the observations in the two BCF₁ populations, and MP represents the average trait value between their corresponding parents. HS: HS46; MAR: MARCABUCAG8US-1-88

Fig. 2

Phenotypic variance explained by the m-QTL and e-QTL effects for yield and yield components. a Phenotypic variance explained by the m-QTLs. PV: the phenotypic variance that the total effects explained; PV (A): the phenotypic variation that the main effect explained; PV (AE): the phenotypic variation that the environmental interaction effect explained. b Phenotypic variance explained by the e-QTLs. PV: the phenotypic variation that the total epistasis effect explained; PV (AA): the phenotypic variation that the main epistasis effect explained; PV (AAE): the phenotypic variation that the environmental interaction of the epistasis effect explained. P₁: RILs; P₂: IF₂s; P₃: HSBCF₁s; P₄: MARBCF₁s; P₅: IF₂MPHs; P₆: HSBCF₁MPHs; P₇: MARBCF₁MPHs