Broomrape, caused by Orobanche cumana, has affected sunflowers since the early 20 th century in Eastern Europe. Currently, it limits sunflower oil production in Southern and Eastern Europe and in some areas of Asia, causing around 50% seed losses when susceptible hybrids are grown. Covered in this review are aspects such as: biological processes that are common to Orobanche spp. and/or particular to O. cumana in sunflower, genetic resistance and its mechanisms, races of the parasite identified in different countries throughout the time and their increasing virulence, and breeding for resistance to some herbicides as a novel control option. The main purpose is to present an updated and, as far as possible, complete picture of the way both the parasitic weed and its host crop have evolved in time, and how they co-exist in the current agriculture. Additionally, we propose a system for determining the races of the parasite that can be internationally adopted from now. In the context of minimal harmful effects on the environment, changing patterns of land use in farming systems, and global environment changes, the final goal of this work is to provide all those interested in parasites from field crops and their integrated management compiled information on the sunflower -O. cumana system as a case study.Additional key words: genes of resistance; Helianthus annuus L.; broomrape; parasite races; virulence. Abbreviations used: AHAS (acetohydroxyacid synthase); GS (germination stimulants); HR (herbicide resistant); IMI (resistance to imidazolinone); PG (polygalacturonases); PME (pectin methyl esterase); POB (pyrimidyloxybenzoates); QTL (quantitative trait loci); SU (sulfonylurea); TZ (triazolopyrimidines).Citation: Molinero-Ruiz, L.; Delavault, P.; Pérez-Vich, B.; Pacureanu-Joita, M.; Bulos, M.; Altieri, E.; Domínguez, J. (2015). History of the race structure of Orobanche cumana and the breeding of sunflower for resistance to this parasitic weed: A review.

A partially dominant nuclear gene conferring resistance to the imidazolinone herbicides was previously identified in the cultivated sunflower (Helianthus annuus L.) line CLHA-Plus developed by seed mutagenesis. The objective of this study was to characterize this resistant gene at the phenotypic, biochemical and molecular levels. CLHA-Plus showed a complete susceptibility to sulfonylureas (metsulfuron, tribenuron and chlorsulfuron) but, on the other hand, it showed a complete resistance to imidazolinones (imazamox, imazapyr and imazapic) at two rates of herbicide application. This pattern was in close association with the AHAS-inhibition kinetics of protein extracts of CLHA-Plus challenged with different doses of imazamox and chlorsulfuron. Nucleotide and deduced amino acid sequence comparisons between resistant and susceptible lines indicated that the imidazolinone-resistant AHAS of CLHA-Plus has a threonine codon (ACG) at position 122 (relative to the Arabidopsis thaliana AHAS sequence), whereas the herbicide-susceptible enzyme from BTK47 has an alanine residue (GCG) at this position. Since the resistance genes to AHAS-inhibiting herbicides so far characterized in sunflower code for the catalytic (large) subunit of AHAS, we propose to redesignate the wild type allele as ahasl1 and the incomplete dominant resistant alleles as Ahasl1-1 (previously Imr1 or Ar ( pur )), Ahasl1-2 (previously Ar ( kan )) and Ahasl1-3 (for the allele present in CLHA-Plus). The higher tolerance level to imidazolinones and the lack of cross-resistance to other AHAS-inhibiting herbicides of Ahasl1-3 indicate that this induced mutation can be used to develop commercial hybrids with superior levels of tolerance and, at the same time, to assist weed management where control of weedy common sunflower is necessary.

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 M2:4 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

The first commercial herbicide-resistant trait in sunflower (Helianthus annuus L.) is known as 'Imisun'. Imidazolinone resistance in Imisun cultivars has been reported to be genetically controlled by a major gene (known as Imr1 or Ahasl1-1) and modifier genes. Imr1 is an allelic variant of the Ahasl1 locus that codes for the acetohydroxyacid synthase, which is the target site of these herbicides. The mechanism of resistance endowed by modifier genes has not been characterized and it could be related to non-target-site resistance. The objective of this study was to evaluate the role of cytochrome P450 monooxygenases (P450s) in Imisun resistance. The response to imazapyr herbicide in combination with P450s inhibitor malathion was evaluated in 2 Imisun

Sunflower rust, caused by Puccinia helianthi Schw., can result in significant yield losses in cultivated sunflower (Helianthus annuus L. var. macrocarpus Ckll.). HAR6 is a germplasm population resistant to most predominant rust races. The objectives of this study were to map the resistance factor present in HAR6 (RHAR6), and to provide and validate molecular tools for the identification of this gene for marker assisted selection purposes. Virulence reaction of seedlings for the F2 population and F2:3 families suggested that a single dominant gene confers rust resistance in HAR6-1, a selected rust resistance line from the original population. Genetic mapping with eight markers covered 97.4 cM of genetic distance on linkage group 13 of the sunflower consensus map. A co-dominant marker ZVG61 is the closest marker distal to RHAR6 at a genetic distance of 0.7 cM, while ORS581, a dominant marker linked in the coupling phase, is proximal to RHAR6 at a genetic distance of 1.5 cM. Validation of these markers was assessed by converting a susceptible line into a rust resistant isoline by means of marker assisted backcrossing. The application of these results to assist the breeding process and to design new strategies for rust control in sunflower is discussed.