Ijaz Siddra, Haq Imran Ul, Razzaq Hafiza Arooj
Centre of Agricultural Biochemistry and Biotechnology (CABB), University of Agriculture, University Road, Faisalabad, Pakistan.
Department of Plant Pathology, University of Agriculture, University Road, Faisalabad, Pakistan.
Physiol Mol Biol Plants. 2023 Jan;29(1):1-10. doi: 10.1007/s12298-022-01273-6. Epub 2022 Dec 26.
We investigated the role of the DDTFR10/A gene of the ethylene response element-binding protein (EREBP) family through the CRISPR/Cas9 genome editing approach. The associated role of this gene in tomato fruit ripening was known. The involvement of ripening-regulatory proteins in plant defense has been documented; therefore, to find the involvement of the DDTFR10/A gene in host susceptibility, we introduced the mutation in DDTFR10/A gene through CRISPR/cas9 in the genome of the tomato plant. The 50% biallelic and 50% homozygous mutations were observed in the T generation. The CRISPR/Cas9 edited plants showed 40% reduced symptoms of Fusarium wilt compared to control plants (non-edited). The DDTFR10/A gene expression in tomato plants was evaluated against biotic (Fusarium wilt) and abiotic (salinity) stresses, and the upregulated expression of this gene was found under both challenges. However, a comparative increase in DDTFR10/A gene expression was observed in tomato plants upon inoculation with f. sp. . The phenotypic assay performed on edited tomato plants demonstrated the role of the DDTFR10/A gene in contributing toward susceptibility against Fusarium wilt.
The online version contains supplementary material available at 10.1007/s12298-022-01273-6.
我们通过CRISPR/Cas9基因组编辑方法研究了乙烯反应元件结合蛋白(EREBP)家族的DDTFR10/A基因的作用。该基因在番茄果实成熟中的相关作用是已知的。成熟调控蛋白参与植物防御已有文献记载;因此,为了探究DDTFR10/A基因在宿主易感性中的作用,我们通过CRISPR/cas9在番茄植株基因组中引入了DDTFR10/A基因突变。在T代中观察到50%的双等位基因突变和50%的纯合基因突变。与对照植株(未编辑)相比,经CRISPR/Cas9编辑的植株枯萎病症状减轻了40%。评估了番茄植株中DDTFR10/A基因在生物(枯萎病)和非生物(盐胁迫)胁迫下的表达,发现在这两种胁迫下该基因均上调表达。然而,在用尖孢镰刀菌接种后,番茄植株中DDTFR10/A基因表达出现了相对增加。对编辑后的番茄植株进行的表型分析证明了DDTFR10/A基因在导致对枯萎病易感性方面的作用。
在线版本包含可在10.1007/s12298-022-01273-6获取的补充材料。