Mechanism analysis of broad-spectrum disease resistance induced by expression of anti-apoptotic p35 gene in tobacco.
- Author:
Zhihua WANG
1
;
Jianhua SONG
;
Yong ZHANG
;
Baoyu YANG
;
Yao WANG
;
Shiyun CHEN
Author Information
1. State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China.
- Publication Type:Journal Article
- MeSH:
Gene Expression Regulation, Plant;
Immunity, Innate;
Plant Diseases;
genetics;
Plants, Genetically Modified;
genetics;
immunology;
virology;
Tobacco;
genetics;
immunology;
virology;
Tobacco Mosaic Virus;
Transformation, Genetic;
Viral Proteins;
genetics;
metabolism
- From:
Chinese Journal of Biotechnology
2008;24(10):1707-1713
- CountryChina
- Language:English
-
Abstract:
Studies have shown that transgenic plants expressing antiapoptotic genes from baculovirus and animals increase resistance to biotic and abiotic stress. However, the mechanism under these resistances is conjectural, or in some cases even controversy. In the present study, the p35 gene from baculovirus Autographa californica multicapsid nucleopolyhedrovirus (AcMNPV) was expressed in tobacco, and for the first time P35 protein was detected in transgenic plants by Western blotting. Inoculation of T1 transgenic tobacco leaves with tobacco mosaic virus (TMV) showed enhanced resistance, and DNA laddering was observed after TMV infection in control but not in transgenic plants. DAB staining showed that TMV infection did not affect peroxide induction of transgenic plants, Western blotting analysis of PR1 protein also showed no difference of control and transgenic plants. Inoculation of fungus (Sclerotinia sclerotiorum) using a detached leaf assay showed enhanced resistance of transgenic leave tissue. RT-PCR analysis demonstrated that p35 gene expression induced earlier expression of PR1 gene after S. sclerotiorum infection. Taken together, our results suggest that the mechanism under enhanced disease resistance by P35 protein is possibly related to the activation of PR-related proteins in addition to the inhibition of programmed cell death, depending on the pathogens challenged.
