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转录组学、代谢组学和激素分析的整合表明,GA 和 CTK 抑制的病斑形成与面包小麦(Triticum aestivum L.)中的细胞死亡和抗病性有关。

Integration of transcriptomics, metabolomics, and hormone analysis revealed the formation of lesion spots inhibited by GA and CTK was related to cell death and disease resistance in bread wheat (Triticum aestivum L.).

机构信息

State Key Laboratory of Crop Gene Exploration and Utilization in Southwest China, Sichuan Agricultural University, Chengdu, China.

Triticeae Research Institute, Sichuan Agricultural University, Chengdu, China.

出版信息

BMC Plant Biol. 2024 Jun 15;24(1):558. doi: 10.1186/s12870-024-05212-3.

DOI:10.1186/s12870-024-05212-3
PMID:38877396
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11179392/
Abstract

BACKGROUND

Wheat is one of the important grain crops in the world. The formation of lesion spots related to cell death is involved in disease resistance, whereas the regulatory pathway of lesion spot production and resistance mechanism to pathogens in wheat is largely unknown.

RESULTS

In this study, a pair of NILs (NIL-Lm5 and NIL-Lm5) was constructed from the BCF population by the wheat lesion mimic mutant MC21 and its wild genotype Chuannong 16. The formation of lesion spots in NIL-Lm5 significantly increased its resistance to stripe rust, and NIL-Lm5 showed superiour agronomic traits than NIL-Lm5 under stripe rust infection.Whereafter, the NILs were subjected to transcriptomic (stage N: no spots; stage S, only a few spots; and stage M, numerous spots), metabolomic (stage N and S), and hormone analysis (stage S), with samples taken from normal plants in the field. Transcriptomic analysis showed that the differentially expressed genes were enriched in plant-pathogen interaction, and defense-related genes were significantly upregulated following the formation of lesion spots. Metabolomic analysis showed that the differentially accumulated metabolites were enriched in energy metabolism, including amino acid metabolism, carbohydrate metabolism, and lipid metabolism. Correlation network diagrams of transcriptomic and metabolomic showed that they were both enriched in energy metabolism. Additionally, the contents of gibberellin A7, cis-Zeatin, and abscisic acid were decreased in leaves upon lesion spot formation, whereas the lesion spots in NIL-Lm5 leaves were restrained by spaying GA and cytokinin (CTK, trans-zeatin) in the field.

CONCLUSION

The formation of lesion spots can result in cell death and enhance strip rust resistance by protein degradation pathway and defense-related genes overexpression in wheat. Besides, the formation of lesion spots was significantly affected by GA and CTK. Altogether, these results may contribute to the understanding of lesion spot formation in wheat and laid a foundation for regulating the resistance mechanism to stripe rust.

摘要

背景

小麦是世界上重要的粮食作物之一。与细胞死亡相关的病斑形成涉及抗病性,而小麦病斑形成的调控途径和对病原体的抗性机制在很大程度上尚不清楚。

结果

本研究利用小麦病变模拟突变体 MC21 及其野生型 Chuannong 16 构建了 BCF 群体的一对 NILs(NIL-Lm5 和 NIL-Lm5)。NIL-Lm5 中病斑的形成显著提高了其对条锈病的抗性,且在条锈病感染下,NIL-Lm5 表现出优于 NIL-Lm5 的农艺性状。此后,对 NILs 进行了转录组(阶段 N:无斑点;阶段 S:仅有少量斑点;阶段 M:大量斑点)、代谢组(阶段 N 和 S)和激素分析(阶段 S),取样均来自田间正常植株。转录组分析表明,差异表达基因富集在植物-病原体互作中,且防御相关基因在病斑形成后显著上调。代谢组分析表明,差异积累的代谢物富集在能量代谢中,包括氨基酸代谢、碳水化合物代谢和脂质代谢。转录组和代谢组的相关网络图谱表明,它们都富集在能量代谢中。此外,在病斑形成过程中,叶片中的赤霉素 A7、顺式玉米素和脱落酸含量降低,而在田间喷施 GA 和细胞分裂素(CTK,反式玉米素)可抑制 NIL-Lm5 叶片中的病斑。

结论

小麦病斑的形成可以通过蛋白质降解途径和防御相关基因的过度表达导致细胞死亡,从而增强对条锈病的抗性。此外,病斑的形成受 GA 和 CTK 的显著影响。总之,这些结果可能有助于理解小麦病斑的形成,并为调控条锈病抗性机制奠定基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e8a/11179392/ed2500433694/12870_2024_5212_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e8a/11179392/e4ec6501491f/12870_2024_5212_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e8a/11179392/e276c44952f1/12870_2024_5212_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e8a/11179392/244f80a8080b/12870_2024_5212_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e8a/11179392/3074149f20e5/12870_2024_5212_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e8a/11179392/9c1e65bda7d7/12870_2024_5212_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e8a/11179392/ed2500433694/12870_2024_5212_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e8a/11179392/e4ec6501491f/12870_2024_5212_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e8a/11179392/e276c44952f1/12870_2024_5212_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e8a/11179392/244f80a8080b/12870_2024_5212_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e8a/11179392/3074149f20e5/12870_2024_5212_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e8a/11179392/9c1e65bda7d7/12870_2024_5212_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e8a/11179392/ed2500433694/12870_2024_5212_Fig6_HTML.jpg

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