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TaCRT3 is a positive regulator of resistance to Blumeria graminis f. sp. tritici in wheat

青梅 白粉病 生物 植物抗病性 烟草 普通小麦 雷氏柄锈菌 基因 植物 细胞生物学 遗传学 染色体
作者
Jianhong Ren,Panpan Song,Ruobing Li,Qiao Wang,Bingjie Zhao,Baotong Wang,Qiang Li
出处
期刊:Phytopathology [Scientific Societies]
标识
DOI:10.1094/phyto-08-23-0276-r
摘要

Wheat powdery mildew, caused by Blumeria graminis f. sp. tritic (Bgt), is one of the most prevalent diseases of wheat worldwide and can lead to severe yield reductions. Identifying genes involved in powdery mildew resistance will be useful for disease resistance breeding and control. Calreticulin (CRT) is a member of a multigene family widely found in higher plants and is associated with a variety of plant physiological functions and defense responses. However, the role of CRT in wheat resistance to powdery mildew remains uncertain. TaCRT3 was identified from the proteomic sequence of an incompatible interaction between the wheat (Triticum aestivum) cultivar Xingmin 318 and the Bgt isolate E09. Following analysis of transient expression of the GFP-TaCRT3 fusion protein in Nicotiana benthamiana leaves, TaCRT3 was localized in the nucleus, cytoplasm, and cell membrane. Transcript expression levels of TaCRT3 were significantly upregulated in the wheat-Bgt incompatible interaction. More critically, knockdown of TaCRT3 using VIGS resulted in attenuated resistance to Bgt in wheat. Histological analysis showed a significant increase in Bgt development in TaCRT3-silenced plants, whereas pathogen-related (PR) gene was significantly downregulated in TaCRT3-silenced leaves. In addition, overexpression of TaCRT3 in wheat enhanced the resistance to powdery mildew, the growth of Bgt was significantly inhibited, and the area of H2O2 near the infection site and the expression of defense-related genes of the salicylic acid (SA)pathway significantly increased. These findings imply that TaCRT3 may act as a disease resistance factor that positively regulates resistance to powdery mildew, during which SA signaling is probably activated.
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