SUMMARY
Sunflower farmers had very few herbicides available for controlling broadleaf weeds. The discovery of wild sunflower populations resistant to the imidazolinone (IMI) and sulfonylurea (SU) herbicide classes gave sunflower breeders the opportunity to create cultivated sunflower hybrids with resistance to these two classes. Germplasm with resistance to both IMI and SU herbicides have been released to sunflower breeders and transferred into commercial varieties. The commercial sunflower hybrids which is resistant to IMI and SU registered in many countries and have been using successfully in sunflower production since 2002, Additionally, these system it is preferred broadly by farmers due to not being GMO without any limitation and restriction. These two herbicides control many of the broadleaf weeds causing yield losses in sunflower. However, IMI herbicide controls both broomrape and many major problem weeds in sunflower planted areas so IMI resistant hybrids use widely than SU resistant ones.
Key Words: Sunflower, herbicide resistance, imidazolinone, sulfonylurea, weed control
INTRODUCTION
Sunflower growers currently lacked effective options for post emergence control of broadleaf weeds in five years ago and had few options for post emergence control of grasses traditionally. IMI and SU herbicides applied post emergence provide both contact and residual control of a broad spectrum of annual grass and broadleaf (Beres et al., 2005). These two herbicide controls susceptible weeds by inhibiting acetohydroxyacid synthase (AHAS), also called acetolactate synthase (ALS) (Kolkman et al, 2004). The wild sunflower population expressed a mutation in the AHAS gene, which made the plant tolerant to applications of the herbicide (Fabie and Miller, 2002).
Wild sunflower populations resistant to both SU and IMI herbicides were discovered firstly in 1996 in Kansas (Al-Khatib et al. 1998) and South Dakota (White et al. 2002) in soybean fields that had been repetitiously treated with herbicides for several seasons. The trait was introduced into the cultivated sunflower lines using conventional plant breeding techniques. This discovery gave to opportunity to sunflower farmers to control the major problem broadleaf weeds (Tranel and Wright, 2002; Tan et al, 2005).
Resistance to AHAS-inhibiting herbicides has greatly increased the spectrum of herbicides for controlling broadleaf weeds in sunflower (Pang et al, 2003). AHAS resistance has been confirmed also in common sunflower from Kansas, South Dakota, Missouri, and Iowa (Heap 2003; White et al. 2003). Genes for resistance to IMI and SU herbicides in sunflower have been introgressed from resistant wild populations into USDA public inbred lines to develop herbicide resistant cultivars and hybrids (Al-Khatib and Miller 2000; Miller and Al-Khatib 2002, 2004). While herbicide resistances populations are probably caused by mutations in AHAS, the specific mutations have not been identified at this time. However, Kolkman et al, (2004) identified two mutations in the sunflower AHAS1 gene that likely provided resistance to AHAS inhibiting herbicides and they discovered an Ala205Val mutation in sunflower lines developed by introgressing into USDA elite inbred lines. The R gene identified by Bruniard and Miller (2001) from ANN-PUR showed partial dominance. A second gene in some genetic backgrounds affected the degree of resistance.
IMIDAZOLINONE (IMI) HERBICIDE RESISTANCE
Imidazolinone herbicides, which include imazapyr, imazapic, imazethapyr, imazamox, etc… control weeds by inhibiting the enzyme AHAS which is a critical enzyme for the biosynthesis of branched-chain amino acids in plants. This resistance to AHAS gene conferring imidazolinone tolerance was discovered in plants through mutagenesis and selection. IMI tolerant maize, wheat, rice, canola and recently sunflower crops which developed using conventional breeding methods commercialized as Clearfield System by BASF from 1992 to the present. This system gives the opportunity to farmers controlling weed wit post emergence herbicides. The planting Imidazolinone-tolerant crops respectively may also prevent rotational crop injury and injury caused by interaction between AHAS resistance herbicides.
Imidazolinone herbicides control a broad spectrum of grass and broadleaf weeds such as Xanthium strumarium, Sinapis arvensis, Chenopodium album, Cirsium arvense, Convolvulus arvensis, Avena spp., Datura stramonium, Amaranthus spp. succefully in sunflower production in the world. Additionally, an IMI herbicide Intervix (Imazamox + Imazapyr (33+15 g/l)) were registered by BASF Co. to control both Orobanche cernua and key weeds in sunflower production in Turkey (Kaya et al., 2004). Broomrape parasite is the biggest problem and limitation factor for yield in Turkey and in Spain. In Trakya region that is the European part of Turkey and has new races of Orobanche infect 70% of sunflower planting areas, the 80 % of sunflower production area. Because of controlling both broomrape and major problem weeds such as cocklebur, the planting areas of IMI resistant hybrids were doubled in recent years.
SULFONYLUREA (SU) HERBICIDE RESISTANCE
First SU resistant lines were developed in similar way with IMI resistance using classical backcrossing method from wild types in Kansas (Miller and Al-Khatib, 2004). On the other hand, genetic diversity of SU resistance was also found in native H. annuus and H. petiolaris populations collected in Colorado, Kansas, Nebraska, South Dakota, and North Dakota. Of the accessions tested, 57% exhibited resistance to tribenuron. More resistance to tribenuron (belong to SU herbicide group) was found in populations collected in Colorado, Kansas, and Nebraska than in North or South Dakota (Olson et al., 2004). These results clearly indicates that tribenuron resistance in wild sunflower is not a new trait, that this resistance was widespread among accessions collected across the provinces of Canada, that resistance occurred in low frequencies in those accessions, and the resistance occurred in the environment before release of SU tolerant sunflower hybrids for commercial production in Canada.
Another SU resistant crop was also developed by Dupont applying chemical mutagenesis and commercial sunflower hybrids released by Pioneer Seed Co. Although 4 IMI resistant sunflower hybrids are commercialized and selling widely in Turkey, none SU resistant hybrids registered yet. The preference of SU herbicide in sunflower production system could be due to less expensive than IMI and broaden control spectrum of weed especially in non-broomrape problem areas.
CROSS RESISTANCE IN SUNFLOWER
Cross-resistance among the common mutations of ALS genes has been reported as early as 1992 (Guttieri et al., 1992). The mutation of ALA205 to VAL at the conserved region AFQEPT of the ALS gene provided higher resistance to the IMI herbicide, Beyond, but only moderately low resistance to SU herbicide, Express (Bruniard, 2001). However, Fabie and Miller (2002) mentioned that USDA source of Express resistance (USDA GH274-1) gave moderately high cross-resistance to the IMI Beyond herbicide, as well as complete resistance to the Express SU herbicide. They also indicated that the conserved region of the ALS gene involved in the USDA SU-resistant germplasm would be the AITGQVPRRMIGT region, or a mutation of the PRO197.
Baumgartner et al. (1999) found that imazethapyr-resistant common sunflower was highly resistant to imazamox, slightly resistant to thifensulfuron and chlorimuron, and not resistant to cloransulam. Resistance ratios of herbicide concentrations required to inhibit growth by 25% were 310, 3.3, 2.0, and 1.4 times greater in the resistant biotype than in the susceptible biotype for imazamox, thifensulfuron, chlorimuron, and cloransulam, respectively. Similarly, herbicide concentrations required to inhibit ALS activity in vitro by 25% were 332.0, 18.6, 8.3, and 1.2 times greater in the resistant biotype than in the sensitive biotype for imazamox, chlorimuron, thifensulfuron, and cloransulam, respectively. White et al. (2002 and 2003) examined ALS-inhibitor resistance biotype and the results indicated that the resistant population required 39 and 9 times more imazethapyr and chlorimuron, respectively, to obtain the same level of enzyme inhibition compared with the sensitive biotype. They suggested that the differences in the common sunflower populations were attributed to an altered site of action on the ALS enzyme.
THE RISKS FOR ENVIRONMENT, HUMANS AND ANIMAL FEEDING
Due to being native crops to America, sunflower is both weed in other growing and growing crop in North America. The discovery of resistance to AHAS-inhibiting herbicides in wild sunflowers has created the basis for deploying herbicide resistant hybrids. The appearance of gene flow from IMI resistant sunflower to wild relatives, the lack of mutation in common sunflower and widespread use of the hybrids could result in emergence of new herbicide-resistant weedy sunflower biotypes by both selection and gene flow (Marshall et al. 2001; Howatt et al. 2003; Massinga et al. 2003).
In normal sunflower crops, IMI herbicides are inhibiting enzymes activity binding to a specific site on the AHAS enzyme. By altering a single amino acid in the AHAS enzyme, scientists have changed this site in such a way that the herbicide cannot bind to it and therefore cannot inhibit the enzyme's activity. Therefore there is no difference between conventional variety and IMI resistance ones for limiting enzyme activity and none allergen effect in the plant (Al-Khatib et al., 1999). However, as cultivated sunflower readily outcrosses with wild relatives, this trait could be transferred to wild sunflower. The being present of various levels of imidazolinone tolerance in wild sunflower populations, being controlled using other types of herbicides to affected wild populations and not giving to IMI sunflower any selective advantage over conventional sunflower; this transfer will have little impact (Marshall et al.2001)
The altered AHAS gene does not significantly affect the plant's biosynthesis of the essential amino acids isoleucine, leucine, and valine. Because only the AHAS enzyme has been changed, there is no any affecting trait for humans, animals including insects in IMI resistant sunflower. For feed safety, the nutritional composition (for example, protein, fat, fibre, amino acids, minerals, and B and E vitamins) of IMI resistant was similar to conventional sunflower. These results also show that alteration of the AHAS gene in sunflower does not affect its composition or nutritional quality.
CONCLUSIONS
The IMI and SU tolerance trait was introgressed from wild types into cultivated sunflower germplasm and released by the USDA. Sunflower seed companies developed hybrids tolerant to the IMI and SU herbicides through conventional breeding approaches. Then, sunflower growers had options for post emergence control of grasses and broadleaf weeds effectively. IMI herbicides both control broomrape and key weeds such as cocklebur efficiently using with resistant IMI hybrids, which is called Clearfield System. This system was preferred and used widely than SU resistant hybrids due to solving both two important problems in sunflower production in the world.
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