Abstract
Fusarium head blight (FHB) has a negative impact on cereal food safety, quality and yield. The majority of FHB resistance genes in wheat (Triticum spp.) have been identified based on reaction to Fusarium graminearum, which, in Canada, has two prevalent trichothecene chemotypes, 3-acetyl-deoxyinvalenol (ADON) and 15-ADON. Three hexaploid (Triticum aestivum L.) and four tetraploid (Triticum turgidum L. ssp. durum and Triticum turgidum L. spp. dicoccoides (Korn. ex Asch. & Graebn.) Thell.) wheat genotypes with different genes for resistance and with different reactions to F. graminearum were evaluated in replicated greenhouse trials to determine if the resistance genes currently deployed in Canadian wheat are effective against both the 3-ADON and 15-ADON chemotypes. The development of FHB was rated as disease severity. The genotypes showed differential responses, with a higher level of disease development in the hexaploid wheat genotypes inoculated with the 3-ADON than with the 15-ADON chemotype. The opposite was observed in the tetraploid wheat genotypes. Tetraploid genotype BGRC3487 and a hexaploid genotype ND2710 showed similar resistance to both 3-ADON and 15-ADON chemotypes. These would be effective sources to breed lines resistant to both 3-ADON and 15-ADON chemotypes and reduce FHB risk.
Résumé
La brûlure de l’épi causée par le fusarium (BEF) a un effet néfaste sur les céréales quant à leur qualité et à leur rendement ainsi qu’à la sécurité alimentaire. Chez le blé (Triticum spp.), la plupart des gènes de résistance à la BEF ont été identifiés en se basant sur la réaction à Fusarium graminearum qui, au Canada, possède deux principaux chimiotypes fondés sur les trichothécènes, soit 3-acétyl-déoxyinvalénol (ADON) et 15-ADON. Trois génotypes de blé hexaploïde (Triticum aestivum L.) et quatre de blé tétraploïde (Triticum turgidum L. ssp. durum and Triticum turgidum L. spp. dicoccoides [Korn. ex Asch. & Graebn.] Thell.) possédant différents gènes de résistance et affichant différentes réactions à F. graminearum ont été évalués dans le cadre d’essais répétés en serre afin de déterminer si les gènes de résistance couramment déployés dans les blés canadiens sont efficaces contre les chimiotypes 3-ADON et 15-ADON. Le développement de la BEF a été évalué en fonction de la gravité de la maladie. Les génotypes ont affiché différentes réactions, y compris un taux plus élevé du développement de la maladie chez les génotypes de blé hexaploïde inoculés avec le chimiotype 3-ADON plutôt qu’avec le 15-ADON. Le contraire a été observé chez les génotypes de blé tétraploïde. Le génotype tétraploïde BGRC3487 et le génotype hexaploïde ND2710 ont affiché une résistance analogue aux deux chimiotypes. Ceux-ci pourraient être efficaces pour développer des lignées résistantes aux deux chimiotypes et réduire les risques engendrés par la BEF.
Introduction
Fusarium head blight (FHB) has become one of the most devastating fungal diseases of wheat in western Canada. The disease develops during anthesis and early kernel development under warm and humid conditions (Gilbert and Tekauz Citation2000). The infected spikes produce shrivelled and discoloured kernels, which reduce grain yield and end-use quality (Dexter et al. Citation1996, Citation1997). The economic value of harvested grain can be further reduced due to grain contamination by Fusarium mycotoxins, which are harmful for both humans and livestock (McMullen et al. Citation1997). Many countries have established maximum allowable levels of mycotoxins in wheat and its products. For example, a maximum mycotoxin level of 1.25 ppm is allowed in bread wheat grain, and 0.5 ppm in bread in the European Union (EU Citation2005).
Genetic resistance remains the most desirable option to manage FHB and reduce mycotoxin contamination. The FHB-resistant hexaploid germplasm currently used in Canadian breeding programmes is derived mainly from spring wheats from China and Brazil, including ‘Sumai 3ʹ, ‘Wangshuibai’, ‘Frontana’ and their derivatives (Gilbert and Tekauz Citation2000; McCartney et al. Citation2016), and winter wheat from Europe (Buerstmayr et al. Citation2009). Sources of FHB resistance are rare in the primary gene pool of tetraploid wheat (Haile et al. Citation2019), but have been identified in both the primary (Sari et al. Citation2018, Citation2020) and secondary (Ruan et al. Citation2012) gene pools of tetraploid wheat. Breeding progress has been hampered in both wheat species by genotype × environment interactions, which may be related to the fact that FHB is caused by multiple Fusarium species. At least 36 Fusarium species have shown association with the occurrence of FHB, and several species co-exist on wheat heads (Parry et al. Citation1995; Bottalico and Perrone Citation2002; Sarver et al. Citation2011; van der Lee et al. Citation2015).
In western Canada, the most common Fusarium species isolated from infected kernels are F. graminearum, F. culmorum, F. poae, F. avenaceum and F. sporotrichioides (Clear and Patrick Citation2000; Gilbert et al. Citation2001; Tekauz et al. Citation2004). Fusarium graminearum Schwabe (teleomorph Gibberella zeae (Schwein.) Petch) is the most prevalent pathogen, but other species are dominant in some regions and can produce high levels of mycotoxins (Clear and Patrick Citation2000; Gilbert and Tekauz Citation2000; Mesterházy et al. Citation2005). Xue et al. (Citation2004) reported that F. graminearum and F. culmorum are most aggressive on wheat, followed by F. sporotrichioides, F. poae and F. avenaceum. FHB resistance in wheat has been verified as neither Fusarium species-specific nor Fusarium isolates-specific (van Eeuwijk et al. Citation1995; Mesterházy et al. Citation2005). Research has focused on wheat genotype reaction to F. graminearum because of its prevalence and its predominance over F. culmorum in wheat production areas (Wilcoxson et al. Citation1992; Tekauz et al. Citation2004; Valverde-Bogantes et al. Citation2020), and the majority of QTL for FHB resistance was identified by the assessment of disease caused by F. graminearum (Anderson et al. Citation2001; Shen et al. Citation2003; Lemmens et al. Citation2005; Ma et al. Citation2006; Ruan et al. Citation2012; Zhang et al. Citation2020).
Many Fusarium species have the ability to produce highly deleterious trichothecene mycotoxins, including deoxynivalenol (DON) and its acetylated forms [3-acetyl-deoxynivalenol (3-ADON), 15-acetyl-deoxynivalenol (15-ADON)], nivalenol (NIV), NX-2, NX-3, NX-4, T-2 toxin and HT-2 toxin (Bottalico Citation1998; Bottalico and Perrone Citation2002; Varga et al. Citation2015). Isolates of Fusarium species are further classified according to the toxigenic characteristic of the dominant trichothecene produced as a 3-ADON, 15-ADON, NIV or NX-2 chemotype (Ichinoe et al. Citation1983; Miller et al. Citation1991; Kelly and Ward Citation2018). Trichothecene mycotoxins are generally believed to act as aggressiveness factors (Langevin et al. Citation2004). Goswami and Kistler (Citation2005) reported that the aggressiveness level of F. graminearum isolates was related to their chemotypes and the level of trichothecene produced. Amarasinghe et al. (Citation2019) characterized 150 strains of F. graminearum collected from eight different countries, including Canada, and found 50% of the strains were 15-ADON, 35% 3-ADON and 15% NIV. NX-2 is an emergent chemotype exclusively found in F. graminearum strains in the northern USA and southern Canada which remain genetically distinct from F. graminearum strains producing other chemotypes (Kelly and Ward Citation2018). Recently, the F. graminearum 3-ADON chemotype has replaced the 15-ADON chemotype as the most prevalent FHB strain in western Canada and USA (Ward et al. Citation2008; Valverde-Bogantes et al. Citation2020). Ward et al. (Citation2008) reported that the frequency of the 3-ADON chemotype, which produces higher levels of trichothecene than the 15-ADON chemotype, increased more than 14-fold between 1998 and 2004 in western Canada. The shift from F. graminearum 15-ADON to 3-ADON has not occurred in eastern Canada (Tamburic-Ilincic et al. Citation2015).
It is not clear whether the FHB resistance genes currently deployed by Canadian wheat breeders are effective against all F. graminearum chemotypes. Indeed, recent research in North Dakota demonstrated greater FHB symptoms and DON production by the 3-ADON than the 15-ADON chemotype in two of three hexaploid wheat genotypes (Puri and Zhong Citation2010), but others found no differences (Gilbert et al. Citation2010; von der Ohe et al. Citation2010). However, there is no information on the effects of the two chemotypes on durum wheat, the most widely cultivated tetraploid wheat.
The objective of this study was to investigate the resistance of hexaploid and tetraploid wheat genotypes to the 3-ADON and 15-ADON chemotypes of F. graminearum to provide information to guide the search for additional QTL and for the development of strategies to breed for FHB resistance.
Materials and methods
The experiment was conducted in a controlled greenhouse environment to avoid confounding effects of other Fusarium isolates and species present in endemic field conditions. Plants were grown in 15-cm pots filled with Terra-Lite Redi-Earth (W.R. Grace and Co. of Canada Ltd., Ajax, ON) and fertilized at the three-leaf stage with 5 g of Osmocote slow release granular fertilizer (14–14-14) (Plant Product Co. Ltd., Brampton, ON), followed by biweekly applications of Plant Products 20–20-20 (N-P-K) all-purpose fertilizer at a rate of 3 g L−1 water. Plants were watered every two days. Growth conditions were set at day/night temperatures of approximately 22/16°C with a 16-h photoperiod.
Three hexaploid and four tetraploid wheat genotypes with different FHB resistance levels were chosen for this experiment (). The hexaploids were ND2710, a Sumai 3-derived genotype with high resistance developed at North Dakota State University (Frohberg et al. Citation2004), ‘AC Barrie’ (McCaig et al. Citation1996) with intermediate resistance derived from the cultivar ‘Frontana’ (Gilbert and Tekauz Citation2000) and the susceptible hard red spring cultivar ‘CDC Teal’ (Hughes and Hucl Citation1993). Both ‘AC Barrie’ and ‘CDC Teal’ are from Canada. The tetraploid genotypes were BGRC3487, DT696, DT735 and ‘AC Morse’. The tetraploid line BGRC3487 (T. dicoccoides), obtained from the Weihenstephan collection of the Braunschweig Genetic Resources Centre in Germany, has a high level of resistance to F. graminearum (Ruan et al. Citation2012; Brar Citation2019). The tetraploid durum (T. durum) breeding lines DT696 from a fortuitous cross with increased resistance and a progeny, DT735 (DT696/AC Avonlea) (Singh et al. Citation2008; Clarke et al. Citation2010), from the Agriculture and Agri-Food Canada, Swift Current durum breeding programme have intermediate resistance, and ‘AC Morse’ is susceptible.
Table 1. Hexaploid and tetraploid wheat genotypes included in this study and their response to Fusarium head blight (FHB)
Two isolates each of 3-ADON and 15-ADON chemotypes of F. graminearum were obtained from Dr. Jeannie Gilbert of the Cereal Research Centre, Agriculture and Agri-Food Canada, Winnipeg, Manitoba. The isolates of the 3-ADON chemotype were M9-04-6 (M9) and M6-04-4 (M6), and those of 15-ADON were M1-04-1 (M1) and M8-04-3 (M8). To produce macroconidia used for inoculation, each isolate was cultured on potato dextrose agar (Difco) for 5–7 d in 9-cm-diam. Petri dishes under continuous fluorescent light at approximately 21°C. After incubation, sterile distilled water was added to the agar surface and gently scraped with a sterile plastic loop. The macroconidial suspension was subsequently filtered through a miracloth with a pore size of 22–25 µm to remove mycelia fragments. A haemocytometer was used to count spores and the suspension was adjusted to 5 × 104 spores mL−1 for the inoculation.
Six fungal treatments consisted of the two 3-ADON and two 15-ADON isolates, mixture one (M6M1) was composed of isolates M6-04-4 and M1-04-1, and mixture two (M9M8) was composed of isolates M9-04-6 and M8-04-3. Mixtures were used to determine if 3-ADON/15-ADON isolates interact during initial infection, resulting in more severe FHB development. Two spikes on each of four plants were inoculated with a single fungal treatment in each genotype. Wheat genotype × fungal chemotype treatments were replicated five times. The experiment was performed three times in the greenhouse, in which there were a total of 120 spikes inoculated for a single fungal treatment in each genotype.
At 50% anthesis (growth stage 65, Zadoks et al. Citation1974), spikes on each plant were inoculated with 10 µL of macroconidial suspension containing 0.02% (v/v) Tween 20 at a concentration of 5 × 104 spores mL−1 for each isolate or mixture. The macroconidial suspension was injected between the lemma and palea of a basal floret of a spikelet. The spikelet position was two-thirds above the base of the spike (Cuthbert et al. Citation2006). The inoculated spike was subsequently covered with a 15 × 8 cm clear Bitran Series S (VWR International, USA) liquid-tight specimen bag to increase the humidity around the spike by transpiration. To secure approximately 100% relative humidity over the spike, the specimen bag was misted with distilled water before covering the spike. Spikes were incubated in the specimen bag for 48 h to aid in FHB symptom development. The severity of FHB was assessed at day 7, 14 and 21 after inoculation and averaged over the four plants for each treatment.
Fusarium head blight severity was rated on a 0 to 5 disease scale (DS) and as percentage of infected spikelets (IS) per spike. The disease scale was described by Murphy et al. (Citation1999) as follows: 0, no infection; 1, inoculated floret infected; 2, inoculated spikelet infected; 3, inoculated spikelet and its rachis infected; 3.2, inoculated and one adjacent spikelet infected; 3.4, inoculated and two adjacent spikelets infected; 3.6, inoculated and three adjacent spikelets infected; 3.8, inoculated and four adjacent spikelets infected; 4, half of a spike infected; 5, a whole spike infected.
The endpoint IS and DS were analysed with mixed models using the PROC MIXED procedure of SAS (Littell et al. Citation1996) for each experiment and over the experiments. Genotype, chemotype, isolate, and their interactions were considered as fixed effects, the DIFF option performed the differences among the levels within each of the fixed factors. Replication, nesting within replication, experiment, and interactions with experiment were considered as random variation. Product-moment correlation between IS and DS least square means was performed.
Results
Genotype, chemotype and genotype × chemotype interaction significantly affected Fusarium disease spread within the spike, measured by IS and DS, and the variation for experiment × genotype was significant (). Examination of the data indicated that the experiment × chemotype interaction was not statistically significant (P > 0.05). The genotype × chemotype interaction was significant, but did not vary significantly over the repeated experiments. The difference among the genotypes appears to be more clearly defined by IS than DS and the correlation among the two traits was high (r = 0.95 at P < 0.0001), so only the IS data are presented.
Table 2. Mixed analysis for disease scale (DS) and percentage of infected spikelets (IS) at the endpoint of Fusarium head blight disease development (day 21)
Averaged over all treatments, the hexaploid genotype ND2710 was comparable to the tetraploid genotype BGRC3487, with a high degree of resistance to FHB disease caused by both chemotypes. The tetraploid genotypes DT696 and DT735, although not as resistant as ND2710 and BGRC3487, were significantly more resistant than ‘AC Barrie’ hexaploid wheat and the susceptible controls ‘CDC Teal’ and ‘AC Morse’ ().
Table 3. Least-squared means of percentage of infected spikelets (%) of hexaploid and tetraploid wheat genotypes in response to 3-acetyl-deoxyinvalenol (ADON) and 15-ADON chemotypes of Fusarium graminearum, and a mixture of the two chemotypes across isolates
Genotypes responded differently to F. graminearum chemotypes (), as indicated by the significant genotype x chemotype interaction that was consistent over the three environments (). In tetraploid wheat, resistance to disease spread by the 3-ADON chemotype was significantly greater (P < 0.05) than 15-ADON in the resistant genotype BGRC3487 except for the first and third experiments, where near equal resistance to both 3-ADON and 15-ADON chemotypes was observed. Similarly the response of intermediate genotypes DT696 and DT735 showed significantly better resistance to disease spread of the 3-ADON than the 15-ADON chemotype except for DT735 in the first experiment. The susceptible genotype ‘AC Morse’ had a susceptible response to disease spread by both 3-ADON and 15-ADON chemotypes, with a tendency of greater susceptibility to 15-ADON. Hexaploid wheat showed the opposite pattern. A trend of more resistance to disease spread by the 15-ADON vs. 3-ADON chemotype was observed in ND2710 (resistant to FHB), which had the highest level of disease spread resistance to both 3-ADON and 15-ADON chemotypes. ‘AC Barrie’ (intermediate FHB resistance) showed significantly better (P < 0.05) resistance to disease spread by the 15-ADON than the 3-ADON chemotype. ‘CDC Teal’ (susceptible to FHB) expressed the susceptible response to disease spread by both 3-ADON and 15-ADON chemotypes, with a tendency of greater susceptibility to 3-ADON. The disease symptoms of the mixed chemotypes were either significantly lower (P < 0.05) than those of 3-ADON and 15-ADON chemotypes alone in both hexaploid and tetraploid wheat regardless of experiment, or not different ().
The aggressiveness of isolates within the 3-ADON and 15-ADON chemotypes were not significantly different in the resistant, intermediate and susceptible genotypes of hexaploid and tetraploid wheat, nor were the two mixtures different from each other (). There was a difference in the aggressiveness of isolates between chemotypes, with a significant difference observed in the intermediate genotypes of hexaploid and tetraploid wheat, and the susceptible genotype of tetraploid wheat. The effects of isolates on genotypes were consistent with their chemotypes in both hexaploid and tetraploid wheat.
Table 4. Effects averaged over experiments for two 3-acetyl-deoxyinvalenol (ADON) isolates, two 15-ADON isolates and two chemotype mixtures of Fusarium graminearum on percentage of infected spikelets (%) for disease response in hexaploid and tetraploid wheat genotypes
Averaged over both experiments and isolates, disease symptoms were greater (P < 0.01) for 3-ADON than for 15-ADON in the hexaploid genotypes. Conversely, greater (P < 0.0001) disease symptoms were observed for 15-ADON vs. 3-ADON in the tetraploid genotypes ().
Discussion
We observed a trend of greater aggressiveness by 3-ADON than 15-ADON chemotypes in the hexaploid genotypes. This is important in the context of the increasing prevalence of the 3-ADON chemotype in western Canada, since hexaploid wheat is produced on approximately 75% of the wheat seeded area. Puri and Zhong (Citation2010) also noted greater symptom development and DON levels for 3-ADON than for the 15-ADON chemotype in a susceptible (‘Grandin’) and a resistant (ND 2710) hexaploid genotype. Similarly, Foroud et al. (Citation2012) observed differences in response to the 3-ADON and 15-ADON chemotypes in moderately resistant, intermediate and moderately susceptible hexaploid genotypes. Gilbert et al. (Citation2010), however, did not find differences in symptoms for a susceptible hexaploid genotype (‘Roblin’) and a moderately resistant genotype (‘5602 HR’) inoculated with the 3-ADON and 15-ADON chemotypes, nor did von der Ohe et al. (Citation2010). ND2710 showed greater FHB symptoms when inoculated with 3-ADON than with 15-ADON in the study by Puri and Zhong (Citation2010); our results showed the same pattern. Similarly, in a study that assessed the aggressiveness of 150 Fusarium strains collected from eight countries on a moderately resistant hexaploid cultivar ‘Carberry’, Amarasinghe et al. (Citation2019) reported higher FHB disease severity, Fusarium damaged kernel percentage, DON production, growth rates, and macroconidia production for 3-ADON than the 15-ADON and NIV chemotype.
In contrast, our results showed lower disease symptoms in the tetraploid genotypes from inoculation with the 3-ADON vs. the 15-ADON chemotype. Although not characterized for chemotype, isolates in studies of F. graminearum by Langevin et al. (Citation2004) and Akinsanmi et al. (Citation2006) showed differential reactions between tetraploid and hexaploid wheat. The present results suggest that the differences in the pathogenicity of isolates on tetraploid and hexaploid wheat may be due to different resistance mechanisms to the chemotypes and the toxins associated with chemotype. Hexaploid wheat has different resistance mechanisms to tetraploid wheat (Buerstmayr et al. Citation2020). The introgression of resistance from hexaploid wheat into tetraploid durum wheat (i.e., adapted tetraploid wheat) can increase FHB resistance in tetraploid durum germplasm (Zhao et al. Citation2018; Brar Citation2019; Ruan et al. Citation2020). Miller and Arnison (Citation1986) demonstrated, by adding 14C-labelled DON to embryo callus culture, that a resistant genotype had the ability to degrade mycotoxin. This suggests that differences in resistance among genotypes may relate to differential degradation of the mycotoxins produced by the 3-ADON and 15-ADON chemotypes. Using a comparative genomics approach, Walkowiak et al. (Citation2015, Citation2016) found variation in the genomes of 3-ADON and 15-ADON chemotypes. This may explain differences in either the aggressiveness of two chemotypes or their interaction with plants, which result in different levels of disease symptoms and DON production among wheat species or genotypes of a wheat species. More evidence is needed, however, to elucidate the mechanism(s) underlying the differential responses of wheat species and genotypes to different chemotypes of Fusarium species, and to identify the possible existence of pathogenic races of chemotypes.
Multiple genes for resistance with different alleles for resistance predominating in different wheat species can explain the differential FHB severity between 3-ADON and 15-ADON chemotypes, as well as the range in resistance across the genotypes that we observed. Major genes for Type II (disease spread or severity) resistance of hexaploid wheat are reported on chromosomes 2AS, 2BL (Zhou et al. Citation2002), 3BS, 3AL, 4B (Anderson et al. Citation2001; Zhou et al. Citation2002), 5A (Buerstmayr et al. Citation2002) and 6BS, 6AS (Anderson et al. Citation2001; Yang et al. Citation2003), and on chromosomes 1A (Sari et al. Citation2018), 2AL, 5AS, 5AL and 6BS (Somers et al. Citation2006; Sari et al. Citation2018; Brar Citation2019), 3B and 7A (Ruan et al. Citation2012; Brar Citation2019) in tetraploid wheat. Serajazari et al. (Citation2019) and Brar et al. (Citation2019) reported that hexaploid wheat genotypes carrying the resistance allele of the Fhb1 locus on 3BS had lower disease in Type II evaluations, regardless of F. graminearum isolate or chemotype. Serajazari et al. (Citation2019) also indicated that the 3-ADON producing isolates were 18% more aggressive than the 15-ADON isolates in Type I (initial infection) assays. There are no reports of major resistance genes identified in tetraploid wheat to F. graminearum. Research to date on FHB resistance genes only considers the pathogenicity of Fusarium species, and neglects the pathogenic differentiation of chemotypes within Fusarium species. Our results suggest that the F. graminearum chemotype response of current FHB resistance QTL should be identified to facilitate selection for appropriate QTL to develop cultivars with resistance to disease caused both by 3-ADON and 15-ADON chemotypes.
The mixture of 3-ADON and 15-ADON chemotypes showed similar aggressiveness to 3-ADON in the tetraploid genotypes (). In the hexaploids, the mixture tended to lower disease with significantly (P < 0.05) lower severity in ‘AC Barrie’ and in the M6/M1 mixture in ‘CDC Teal’, similar to the results reported by Brar et al. (Citation2019). Miedaner et al. (Citation2004) noted a similar pattern in F. culmorum, wherein aggressiveness was lower in mixtures of isolates than for isolates applied individually in winter rye (Secale cereale L.). Guerrieri (Citation2011), however, found no difference in area under the disease progress curve for the same isolates used in this study when applied as a single mixture to hexaploid genotypes including ‘AC Barrie’ and ‘CDC Teal’. It appears that the variable response to the chemotype mixture observed here was at least partly due to the host-pathogen interaction rather than competition among the chemotypes alone, given the difference in response among genotypes. The chemotype mixture was perhaps more effective in eliciting the host resistance reaction in the intermediate and susceptible hexaploid genotypes than in ND2710 or the tetraploids. A recent study by Serajazari et al. (Citation2019) indicated the lack of interaction between F. graminearum chemotypes and hexaploid wheat genotypes, suggesting that screening of germplasm for resistance could be performed with a limited number of aggressive isolates.
The similar resistance to disease spread displayed by ND2710 and BGRC3487 to different 3-ADON and 15-ADON isolates in this study agrees with other studies. In a study to identify spike culture derived wheat variants exhibiting resistance to disease spread by multiple chemotypes of F. graminearum, Huang et al. (Citation2019) identified five out of 55 lines that conferred resistance to multiple chemotypes. This suggests the possibility to develop wheat genotypes that have resistance to more than one F. graminearum chemotype. The level of resistance and type of wheat genotype under cultivation likely contribute to changes in FHB chemotype populations as well as pathogen population shifts over time. For example, ‘AC Barrie’ showed higher susceptibility to 3-ADON producing F. graminearum strains than 15-ADON. Growing wheat varieties with the ‘AC Barrie’ type of resistance over a large portion of a wheat production region may increase the frequency of the 3-ADON chemotype over the 15-ADON chemotype (Ward et al. Citation2008), and vice versa by growing ‘AC Morse’ type of varieties. In another study that investigated the variation of acetyl ester derivatives of DON in 15 locations in Manitoba following the shift of FHB strains in North America, Guo et al. (Citation2008) described the potential causes for the chemotype shifting as sexual recombination, population age, and cropping system, which could result in genetic and chemotypic diversity. Guo et al. (Citation2008) additionally emphasized the significance of wheat seed shipment and long-distance spore transportation of F. graminearum in contributing to changes in the distribution of chemotype populations. According to Valverde-Bogantes et al. (Citation2020), the shift from F. culmorum to F. graminearum that occurred in Europe was associated with climate change and increased maize production. In a study by Burlakoti et al. (Citation2017), 96% of F. graminearum isolates from maize and 98% of F. graminearum isolates from wheat were of the 15-ADON chemotype in eastern Canada. Interestingly, all F. graminearum isolates from wheat were collected by Burlakoti et al. (Citation2017) from winter common wheat and winter durum wheat. As winter wheat predominates in eastern Canada, and spring wheat predominates in western Canada, this indicated that wheat type (i.e., host) may affect the distribution of F. graminearum chemotypes. Furthermore, effects of climate differences on the distribution of F. graminearum chemotypes were detected for spring wheat (Prodi et al. Citation2011) but not winter wheat (Crippin et al. Citation2020).
Our results indicate that the current shift in prevalence of the F. graminearum 3-ADON over the 15-ADON chemotype in Canada could result in greater FHB risk in some hexaploid genotypes, but possibly reduced FHB severity in tetraploid durum genotypes. The genotype x chemotype interactions observed in this and other studies suggest that the response to the two chemotypes should be investigated in a broader range of host genotypes and environments, to determine those at greatest risk. The tetraploid BGRC3487 and the hexaploid ND2710 showed similar resistance to disease spread by both the 3-ADON and 15-ADON chemotypes, and would thus be useful for breeding of resistant cultivars.
Acknowledgements
We thank Dr. Jeannie Gilbert for providing isolates of F. graminearum.
Additional information
Funding
References
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