Transgressive segregation and maternal genetic effects of non–target site fluazifop-P-butyl tolerance in Zoysia spp.

Abstract

Zoysia germplasm exhibit different levels of sensitivity to fluazifop-P-butyl, but the genetic factors responsible for such differences are unknown. Segregation patterns of the fluazifop-P-butyl tolerance trait were studied under greenhouse conditions. In total, 244 F1 lines were generated from multiple crosses between the tolerant line 5337-2 (non–target site tolerance) and three more-sensitive lines (123, 252, and 5330-23). Progeny segregation showed that fluazifop-P-butyl tolerance within zoysiagrass (Zoysia spp.) is expressed as a quantitative trait with a wide range of intermediate phenotypes between parental phenotypes. Transgressive segregation was extensive and largely favored susceptibility in most families, but was especially evident for 5337-2 × 123 and 5337-2 × 5330-23. The segregation patterns for biomass reduction and percent injury were different within reciprocal crosses and among three different family crosses. Reciprocal effects were observed in growth reduction for 5337-2 × 5330-23, in percent injury at 3 wk after the treatment (WAT), and for 5337-2 × 252 at 6 WAT. This indicated that fluazifop-P-butyl tolerance was not completely controlled by nuclear genetic factors in 5337-2 and maternal/cytoplasmic inheritance was also partially responsible. These results suggested that fluazifop-P-butyl tolerance may be attributed to multiple genetic mechanisms, which could present a challenge for future breeding efforts because of the difficulty of fixing multiple traits within a breeding population.

Confirmation and inheritance of glufosinate resistance in an Amaranthus palmeri population from North Carolina

“…( 2022 ) found the chloroplast GS isoform was overamplified in a glufosinate‐resistant A. palmeri population from Missouri, which provided evidence that there was a resistance mechanism that could be maternally inherited (Reboud & Zeyl, 1994 ). While a more elaborate crossing design (i.e., more genotypes/crosses and glufosinate rates tested) could reflect a more precise number of loci responsible for the mechanism(s) of resistance and the influence of maternally inherited gene(s) conferring variation in phenotype, the presented results provide an efficient approach of determining the inheritance and number of loci involved with glufosinate resistance in the Anson County population (Gressel, 2009 ; Kohlhase et al., 2018 ; Liu et al., 2019 ). Future research should focus on determining the exact mechanism(s) of resistance in the Anson County population.…”