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CROP BREEDING & GENETICS

Genetic Analysis of an Induced Mutation Conferring Imidazolinone Resistance in Sunflower

Biotechnology Dep., NIDERA S.A., Casilla de Correo 6, 2600 Venado Tuerto, Santa Fe, Argentina

^* Corresponding author (csala{at}nidera.com.ar).

Weeds negatively impact sunflower (Helianthus annuus L.) yields and to date few mutants conferring herbicide tolerance have been developed. Our objectives were to identify, characterize, and determine the inheritance of herbicide resistance in a new imidazolinone-resistant mutation-derived sunflower line. This line was obtained through ethyl methanesulfonate mutagenesis of seeds and selection with imazapyr herbicide {2-[(RS)-4-isopropyl-4-methyl-5-oxo-2-imidazolin-2-yl]nicotinic acid} from an M₂ population of nearly 600,000 plants. An M_2:4 line homozygous for the trait was selected for genetic studies and was designated as CLHA-PLUS. This mutant line possesses higher levels of tolerance to imazapyr and imazamox {2-[(RS)-4-isopropyl-4-methyl-5-oxo-2-imidazolin-2-yl]-5-methoxymethylnicotinic acid} than that observed in sunflower lines carrying the already described gene Imr1 which traced back to wild populations. On the basis of analysis of F₁, F₂, and BC₁F₁ populations, it was concluded that resistance in CLHA-PLUS is inherited as a single, partially dominant nuclear gene. An allelism test performed with two different herbicide application rates and a cosegregation test of resistance to a perfect simple sequence repeat marker for the AHASL1 gene of sunflower permitted us to conclude that the mutation present in CLHA-PLUS is different from Imr1 and that both of them are allelic variants of the locus AHASL1.

Abbreviations: AHAS, acetohydroxyacid synthase • AHASL, AHAS large subunit gene • IMI, imidazolinone • I, intermediate • PCR, polymerase chain reaction • R, resistant • S, susceptible • SSR, simple sequence repeats • SUs, sulfonylureas