Mutation of a histidine-rich calcium-binding-protein gene in wheat confers resistance to Fusarium head blight

Li, Guoqiang; Zhou, Jianglin; Jia, Haiyan; Gao, Zhipeng; Fan, Min; Luo, Yan-Jun; Zhao, Pan-Ting; Xue, Shulin; Li, Na; Yuan, Yang; Ma, Shengwei; Kong, Zhongxin; Li, Jia; An, Xia; Jiang, Ge; Liu, Wenxing; Cao, Wenjin; Zhang, Rongrong; Fan, Jicai; Xu, Xiaoyu; Liu, Yanfang; Kong, Qianqian; Zheng, Shouhang; Wang, Yao; Qin, Bin; Cao, Shouyang; Ding, Yang; Shi, Jinxing; Yan, Haisheng; Wang, Xin; Ran, Congfu; Ma, Zhengqiang

doi:10.1038/s41588-019-0426-7

Cited by 197 publications

(166 citation statements)

References 47 publications

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“…Qfhs.nau-6B (Fhb2), Qfhi.nau-4B (Fhb4), and Qfhi.nau-5A (Fhb5) were fine mapped in the 2.2 cM, 0.14 cM, and 0.09 cM interval [16]. Fhb1 has been cloned recently [18][19][20]. In current study, four loci (28 MTAs) were identified on chromosomes 1B, 4A, 5D and 7A in two seasons.…”

Section: Fhb Resistance Loci Identified By Gwasmentioning

confidence: 59%

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Genome-wide association mapping revealed syntenic loci QFhb-4AL and QFhb-5DL for Fusarium head blight resistance in common wheat (Triticum aestivum L.)

Gao

et al. 2020

BMC Plant Biol

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Background: Fusarium head blight (FHB), primarily caused by Fusarium graminearum, is a major threat to wheat production and food security worldwide. Breeding stably and durably resistant cultivars is the most effective approach for managing and controlling the disease. The success of FHB resistance breeding relies on identification of an effective resistant germplasm. We conducted a genome-wide association study (GWAS) using the highdensity wheat 90 K single nucleotide polymorphism (SNP) assays to better understand the genetic basis of FHB resistance in natural population and identify associated molecular markers.Results: The resistance to FHB fungal spread along the rachis (Type II resistance) was evaluated on 171 wheat cultivars in the 2016-2017 (abbr. as 2017) and 2017-2018 (abbr. as 2018) growing seasons. Using Illumina Infinum iSelect 90 K SNP genotyping data, a genome-wide association study (GWAS) identified 26 loci (88 marker-trait associations), which explained 6.65-14.18% of the phenotypic variances. The associated loci distributed across all chromosomes except 2D, 6A, 6D and 7D, with those on chromosomes 1B, 4A, 5D and 7A being detected in both years. New loci for Type II resistance were found on syntenic genomic regions of chromsome 4AL (QFhb-4AL, 621.85-622.24 Mb) and chromosome 5DL (QFhb-5DL, 546.09-547.27 Mb) which showed high collinearity in gene content and order. SNP markers wsnp_JD_c4438_5568170 and wsnp_CAP11_c209_198467 of 5D, reported previously linked to a soil-borne wheat mosaic virus (SBWMV) resistance gene, were also associated with FHB resistance in this study. Conclusion: The syntenic FHB resistant loci and associated SNP markers identified in this study are valuable for FHB resistance breeding via marker-assisted selection.

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Section: Fhb Resistance Loci Identified By Gwasmentioning

confidence: 59%

“…Fhb1 was reported as a pore-forming toxin-like gene (PFT) QTL [18]. However, recent studies revealed an histidine-rich calcium-binding protein (His) was responsible for the Fhb1 resistance [19,20]. A comprehensive discussion on the two studies has been performed, and the nature of Fhb1 resistance remains unclear [21].…”

Section: Introductionmentioning

confidence: 99%

Genome-wide association mapping revealed syntenic loci QFhb-4AL and QFhb-5DL for Fusarium head blight resistance in common wheat (Triticum aestivum L.)

Gao

et al. 2020

BMC Plant Biol

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“…The disease results in yield and quality reductions as well as the contamination of the grains with mycotoxins, particularly trichothecenes, making the crops unsafe for consumption (Desjardins and Proctor 2007;Chen et al 2019). Sources for Fusarium head blight resistance are limited, and fully resistant cultivars to FHB are not yet available and only one resistance locus Fhb1 (containing a debatable resistance gene PFT and a causative gene His/TaHRC) has thus far been cloned in wheat (Rawat et al 2016;Li et al 2019;Su et al 2019). Therefore, a thorough investigation of the mechanisms involved in F. graminearum proliferation and subsequent colonization of its host cells will help in devising effective means of controlling FHB.…”

Section: Introductionmentioning

confidence: 99%

Spatiotemporal nature of Fusarium graminearum-wheat coleoptile interactions

et al. 2019

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Fusarium head blight (FHB) caused by the ascomycete fungus Fusarium graminearum can result in significant crop losses and render the crops harmful to human health due to contamination with mycotoxin. Although the pathogenesis of F. graminearum is widely investigated by molecular genetics approaches, detailed studies about its cellular and developmental processes at the initial stages of infection are very limited. We applied live-cell imaging approach to characterize the spatial and temporal development of growing hyphae and plant responses during F. graminearum and wheat coleoptile interactions. The present investigation demonstrates that F. graminearum uses two strategies to penetrate the host epidermal cells. The pathogen breaks through the host cell wall with appressoria-like structures derived from surficial hyphae, and also with the narrow pegs from thick and bulbous intracellular hyphae. Live cell imaging in the presence of the endocytic tracker FM4-64 showed that the plasma and intermembranes of the invaded wheat coleoptile cells were intact. Invasive hyphae exhibit branching, budding, pseudohyphae-like growth, cell-to-cell spreading ability, and were sealed within a plant membrane, indicating a biotrophic lifestyle of this fungus inside the invaded cells. Time-lapse imaging suggested that there were callose depositions at the plant cell walls in the form of continuous lines and also on the outer linings of the fungal invasive hyphae at colonization stage. In addition, our studies demonstrate that the activation of the toxisomerelated gene (TRI4) requires external stimuli and is spatio-temporally modulated. Generally, this study provides new insights into the colonization strategies and host response features during F. graminearum-plant interactions. Further tracing of cellular details will significantly contribute to our understanding of molecular mechanisms of F. graminearum-host interactions.

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“…Qfhs.nau-6B (Fhb2), Qfhi.nau-4B (Fhb4), and Qfhi.nau-5A (Fhb5) were successfully fine mapped in the 2.2 cM, 0.14 cM, and 0.09 cM interval [16]. Fhb1 has been cloned recently [18][19][20]. In current study, four loci (28 MTAs) were identified on chromosomes 1B, 4A, 5D and 7A in two seasons.…”

Section: Fhb Resistance Loci Identified By Gwasmentioning

confidence: 68%

Genome-wide association mapping revealed syntenic loci QFhb-4AL and QFhb-5DL for Fusarium head blight resistance in common wheat (Triticum aestivum L.)

Hu¹,

Gao²,

Wu³

et al. 2019

Preprint

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Background: Fusarium head blight (FHB), primarily caused by Fusarium graminearum, is a major threat to wheat production and food security worldwide. Breeding stably and durably resistant cultivars is the most effective approach for managing and controlling the disease. The success of FHB resistance breeding relies on identification of an effective resistant germplasm. We performed a genome-wide association study (GWAS) using the high-density wheat 90K single nucleotide polymorphism (SNP) assays to better understand the genetic basis of FHB resistance in natural population and identify associated molecular markers. Results: The resistance to FHB fungal spread along the rachis (Type II resistance) was evaluated on 171 wheat cultivars in the 2016-2017 (abbr. as 2017) and 2017-2018 (abbr. as 2018) growing seasons. Using Illumina Infinum iSelect 90K SNP genotyping data, a genome-wide association study (GWAS) identified 26 loci (88 marker-trait associations), which explained 6.65-14.18% of the phenotypic variances. The associated loci distributed across all chromosomes except 2D, 6A, 6D and 7D, with those on chromosomes 1B, 4A, 5D and 7A being detected in both years. New loci for Type II resistance were found on syntenic genomic regions of chromsome 4AL (QFhb-4AL, 621.85-622.24 Mb) and chromosome 5DL (QFhb-5DL, 546.09-547.27 Mb) which showed high collinearity in gene content and order. SNP markers wsnp_JD_c4438_5568170 and wsnp_CAP11_c209_198467 of 5D, reported previously linked to a soil-borne wheat mosaic virus (SBWMV) resistance gene, were also associated with FHB resistance in this study. Conclusion: The syntenic FHB resistant loci and associated SNP markers identified in this study are valuable for FHB resistance breeding via marker-assisted selection.

show abstract

Mutation of a histidine-rich calcium-binding-protein gene in wheat confers resistance to Fusarium head blight

Cited by 197 publications

References 47 publications

Genome-wide association mapping revealed syntenic loci QFhb-4AL and QFhb-5DL for Fusarium head blight resistance in common wheat (Triticum aestivum L.)

Genome-wide association mapping revealed syntenic loci QFhb-4AL and QFhb-5DL for Fusarium head blight resistance in common wheat (Triticum aestivum L.)

Spatiotemporal nature of Fusarium graminearum-wheat coleoptile interactions

Genome-wide association mapping revealed syntenic loci QFhb-4AL and QFhb-5DL for Fusarium head blight resistance in common wheat (Triticum aestivum L.)

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