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. 2013 Feb;6(2):231-42.
doi: 10.1111/j.1752-4571.2012.00282.x. Epub 2012 Jul 12.

Evolved polygenic herbicide resistance in Lolium rigidum by low-dose herbicide selection within standing genetic variation

Roberto Busi  1 , Paul Neve, Stephen Powles
Affiliations

Evolved polygenic herbicide resistance in Lolium rigidum by low-dose herbicide selection within standing genetic variation

Roberto Busi et al. Evol Appl. 2013 Feb.

Abstract

The interaction between environment and genetic traits under selection is the basis of evolution. In this study, we have investigated the genetic basis of herbicide resistance in a highly characterized initially herbicide-susceptible Lolium rigidum population recurrently selected with low (below recommended label) doses of the herbicide diclofop-methyl. We report the variability in herbicide resistance levels observed in F1 families and the segregation of resistance observed in F2 and back-cross (BC) families. The selected herbicide resistance phenotypic trait(s) appear to be under complex polygenic control. The estimation of the effective minimum number of genes (N E), depending on the herbicide dose used, reveals at least three resistance genes had been enriched. A joint scaling test indicates that an additive-dominance model best explains gene interactions in parental, F1, F2 and BC families. The Mendelian study of six F2 and two BC segregating families confirmed involvement of more than one resistance gene. Cross-pollinated L. rigidum under selection at low herbicide dose can rapidly evolve polygenic broad-spectrum herbicide resistance by quantitative accumulation of additive genes of small effect. This can be minimized by using herbicides at the recommended dose which causes high mortality acting outside the normal range of phenotypic variation for herbicide susceptibility.

Keywords: Mendelian segregation; additive genes; evolution; inheritance; polygenic resistance.

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Figures

Figure 1
Figure 1
Survival response to a range of doses of diclofop-methyl for resistant parental lines (R) (solid circles and dotted line), susceptible original parental line (S) (open circles and solid line), F1 no. 5 (♂ solid squares and solid line), (♀ open squares and short-dashed line) (A); F1 no. 6 (♂ solid squares and solid line), (♀ open squares and short-dashed line) (B); F2 family no.5 (C); F2 family no. 6 (D); type L (grey triangle up and dotted lines), type M (grey triangle down and dash-dotted lines) and type H (grey diamonds and short-dashed line). back-cross (BC) no. 5 (E) and BC no. 6 (F) (open squares and short-dashed line). Symbols are mean of observed plant survival ± SE (n = 3). Lines are estimated plant survival following nonlinear regression analysis.
Figure 2
Figure 2
Variability in survival of 20 cloned F1 plants treated with 188 (Low; white bars), 375 (Medium; grey bars) and 1500 (High; black bars) g diclofop-methyl ha−1. Surviving cloned plants were employed to generate type L, M, H F2 lines in different pair crosses.
Figure 3
Figure 3
Cross-resistance between diclofop-methyl and chlorsulfuron observed in parental R and F1, H F2 families following treatments with the recommended dose of diclofop-methyl (375 g ha−1; white bars) or chlorsulfuron (30 g ha−1; black bars).
See this image and copyright information in PMC

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