共 1 条
Suppression of TGA2-Mediated Salicylic Acid Defence by Tomato Yellow Leaf Curl Virus C2 via Disruption of TCP7-Like Transcription Factor Activity in Tobacco
被引:0
作者:
Li, Ping
[1
,2
]
Zhang, Lei
[1
]
Yan, Xiao-Tian
[1
]
Zheng, Chao
[1
]
Zhang, Xin-Yue
[2
]
Chen, Jian-Ping
[1
]
Liu, Shu-Sheng
[2
]
Wang, Xiao-Wei
[1
,2
]
机构:
[1] Ningbo Univ, Inst Plant Virol, Key Lab Biotechnol Plant Protect MARA, Zhejiang Key Lab Green Plant Protect,State Key Lab, Ningbo, Peoples R China
[2] Zhejiang Univ, Inst Insect Sci, Minist Agr, Key Lab Mol Biol Crop Pathogens & Insects, Hangzhou, Peoples R China
基金:
美国国家科学基金会;
关键词:
begomovirus;
<italic>Bemisia tabaci</italic>;
salicylic acid;
TCPs;
<italic>TGA2</italic>;
SYSTEMIC ACQUIRED-RESISTANCE;
ISOCHORISMATE-SYNTHASE;
DNA-BINDING;
PLANT;
NPR1;
EXPRESSION;
VECTOR;
ACCUMULATION;
SPECIFICITY;
ACTIVATION;
D O I:
10.1111/pce.15411
中图分类号:
Q94 [植物学];
学科分类号:
071001 ;
摘要:
Tomato yellow leaf curl virus (TYLCV) is a significant threat to tomato cultivation globally, transmitted exclusively by the whitefly Bemisia tabaci. While previous research suggests that the TYLCV C2 protein plays a role in fostering mutualistic interactions between the virus and its insect vectors, the specific mechanisms remain unclear. In this study, we show that the C2 protein interferes with the salicylic acid (SA) defence pathway by disrupting TCP7-like transcription factor-mediated regulation of TGA2 expression. Whitefly infestation increases the expression of TCP7-like transcription factors (TCP7-L1 and TCP7-L2), which subsequently trigger TGA2-dependent activation of BGL2 transcription, enhancing plant resistance to whiteflies. However, the TYLCV C2 protein interacts with these TCP7-like factors, reducing their binding affinity to the TGA2 promoter, which in turn suppresses BGL2 expression in the SA signalling pathway. These findings provide new insights into how TYLCV C2 modulates TCP7-like protein activity to impair SA-mediated defences, contributing to the mutualistic relationship between TYLCV and whiteflies. This work deepens our understanding of the complex regulatory networks underlying these virus-vector-host interactions.
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页码:4039 / 4050
页数:12
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