Cauliflower mosaic virus Tav protein induces leaf chlorosis in transgenic tobacco through a host response to virulence function of Tav

• Published in: Journal of general plant pathology : JGPP Vol. 81; no. 4; pp. 261 - 270
• Main Authors: Waliullah, Sumyya, Kosaka, Naomi, Yaeno, Takashi, Ali, Md. Emran, Sekine, Ken-Taro, Atsumi, Go, Yamaoka, Naoto, Nishiguchi, Masamichi, Takahashi, Hideki, Kobayashi, Kappei
• Format: Journal Article
• Language: English
• Published: Tokyo Springer Japan 01-07-2015; Springer Nature B.V
• Subjects: Agriculture; Biomedical and Life Sciences; Cauliflower mosaic virus; cell death; chlorosis; gene expression; Host Responses; hypersensitive response; leaves; Life Sciences; Microbiology; Pathogenesis; pathogenesis-related proteins; Plant diseases; Plant Pathology; plant viruses; Proteins; RNA interference; salicylic acid; Tobacco; Tomato bushy stunt virus; Tomatoes; transactivators; transgenes; Transgenic plants; virulence; Chlorosis; Host response; PR-protein; Pathogenesis; Defense
• ISSN: 1345-2630; 1610-739X
• DOI: 10.1007/s10327-015-0600-4

To study the precise mechanisms underlying the chlorosis caused by plant viruses, we previously established a synchronous experimental system using transgenic plants expressing Cauliflower mosaic virus multifunctional protein, Tav (transactivator/viroplasmin), under the control of an artificially inducible promoter. Shortly after the induction of Tav expression, pathogenesis-related protein (PR) 1a gene expression is upregulated in the transgenic tobacco lines, which show visible chlorosis within a week. The present study showed that the expression of Tav also induces some salicylic acid (SA)- and ethylene-responsive PR genes. In contrast to transiently expressed Tav, which suppressed Agrobacterium-induced and SA-induced PR1a expression, the artificial induction of Tav from the transgene did not affect SA-induced PR1a expression, rather it alone induced PR1a expression. In a deletion analysis, chlorosis and PR1a induction function in transgenic tobacco were mapped to a region in Tav that had been shown to have a role in pathogenesis in a susceptible host, elicitation of the hypersensitive response in a resistant host, suppression of RNA silencing, and the suppression of Tomato bushy stunt virus P19-mediated cell death in tobacco. The results suggest that Tav-induced chlorosis results from a host response, which accompanies PR1a induction, to pathogenic function of Tav.