Cucumber mosaic virus coat protein induces the development of chlorotic symptoms through interacting with the chloroplast ferredoxin I protein

• Published in: Scientific reports 2018-01, Vol.8 (1), p.1205-11, Article 1205
• Main Authors: Qiu, Yanhong, Zhang, Yongjiang, Wang, Chaonan, Lei, Rong, Wu, Yupin, Li, Xinshi, Zhu, Shuifang
• Format: Article
• Language: English
• Subjects: 14/19; 38/89; 631/326/596/2557; 631/449/2169/2673; 82/111; 82/83; Capsid Proteins - metabolism; Chloroplasts; Chloroplasts - metabolism; Chlorosis; Coat protein; Cucumovirus - physiology; Cytoplasm; Ferredoxin; Ferredoxins - metabolism; Host plants; Host-Pathogen Interactions; Humanities and Social Sciences; Models, Biological; multidisciplinary; Phenotype; Plant Diseases - virology; Plant virus diseases; Protein Binding; Protein Transport; Proteins; Science; Science (multidisciplinary); Tobacco; Viral infections; Yeasts
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-018-19525-5

Cucumber mosaic virus (CMV) infection could induce mosaic symptoms on a wide-range of host plants. However, there is still limited information regarding the molecular mechanism underlying the development of the symptoms. In this study, the coat protein (CP) was confirmed as the symptom determinant by exchanging the CP between a chlorosis inducing CMV-M strain and a green-mosaic inducing CMV-Q strain. A yeast two-hybrid analysis and bimolecular fluorescence complementation revealed that the chloroplast ferredoxin I (Fd I) protein interacted with the CP of CMV-M both in vitro and in vivo , but not with the CP of CMV-Q. The severity of chlorosis was directly related to the expression of Fd1, that was down-regulated in CMV-M but not in CMV-Q. Moreover, the silencing of Fd I induced chlorosis symptoms that were similar to those elicited by CMV-M. Subsequent analyses indicated that the CP of CMV-M interacted with the precursor of Fd I in the cytoplasm and disrupted the transport of Fd I into chloroplasts, leading to the suppression of Fd I functions during a viral infection. Collectively, our findings accentuate that the interaction between the CP of CMV and Fd I is the primary determinant for the induction of chlorosis in tobacco.