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Eureka lemon zinc finger protein ClDOF3.4 interacts with citrus yellow vein clearing virus coat protein to inhibit viral infection

Ping Liao, Ting Zeng, Mengyang Huangfu, Cairong Zheng, Jiequn Ren, Changyong Zhou, Yan Zhou
2024, 23 (6): 1979-1993.   DOI: 10.1016/j.jia.2024.03.049
Abstract81)      PDF in ScienceDirect      
Citrus yellow vein clearing virus (CYVCV) is a new citrus virus that has become an important factor restricting the development of China’s citrus industry, and the CYVCV coat protein (CP) is associated with viral pathogenicity.  In this study, the Eureka lemon zinc finger protein (ZFP) ClDOF3.4 was shown to interact with CYVCV CP in vivo and in vitro.  Transient expression of ClDOF3.4 in Eureka lemon induced the expression of salicylic acid (SA)-related and hypersensitive response marker genes, and triggered a reactive oxygen species burst, ion leakage necrosis, and the accumulation of free SA.  Furthermore, the CYVCV titer in ClDOF3.4 transgenic Eureka lemon plants was approximately 69.4% that in control plants 6 mon after inoculation, with only mild leaf chlorotic spots observed in those transgenic plants.  Taken together, the results indicate that ClDOF3.4 not only interacts with CP but also induces an immune response in Eureka lemon by inducing the SA pathways.  This is the first report that ZFP is involved in the immune response of a citrus viral disease, which provides a basis for further study of the molecular mechanism of CYVCV infection.
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Vesicular transport-related genes in Diaphorina citri are involved in the process of Candidatus Liberibacter asiaticus infection
Yingzhe Yuan, Tao Peng, Aijun Huang, Jun He, Chenyang Yuan, Tianyuan Liu, Long Yi, Xuejin Cui, Xuefeng Wang, Changyong Zhou
2024, 23 (12): 4136-4146.   DOI: 10.1016/j.jia.2024.03.063
Abstract81)      PDF in ScienceDirect      
Asian citrus psyllid (ACP, Diaphorina citri) is the major vector of Candidatus Liberibacter asiaticus (CLas), which is a bacterial pathogen causing the devastating citrus Huanglongbing (HLB) disease.  Diaphorina citri is known to carry CLas in a persistent and propagative manner.  Some studies have suggested that CLas may use the vesicular structures of Dcitri cells as its propagation organelles.  However, the mechanisms by which CLas enters the Dcitri cells and how vesicle-mediated trafficking is involved remain unclear.  In this study, we monitored the titer change of CLas in Dcitri nymphs during the process of CLas acquisition from feeding on infected citrus plants.  We found that the titer of CLas increased with the acquisition access period.  After infection, there was a significant upregulation in the expression of several vesicular transport-related genes in Dcitri.  The titer of CLas was significantly reduced in the midgut and whole insect body when endocytosis and the endosome network in Dcitri were inhibited.  Furthermore, silencing the Dcitri clathrin-heavy chain gene also led to a reduction in the CLas titer in Dcitri.  These results suggest that CLas infection upregulates the genes related to vesicular transport in Dcitri, which facilitates the invasion of endocytosis-dependent pathogens.
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