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The de novo Biosynthesis of Vitamin B6 Is Required for Disease Resistance Against Botrytis cinerea in Tomato

July 2014 , Volume 27 , Number  7
Pages  688 - 699

Yafen Zhang, Bo Liu, Xiaohui Li, Zhigang Ouyang, Lei Huang, Yongbo Hong, Huijuan Zhang, Dayong Li, and Fengming Song

National Key Laboratory for Rice Biology, Institute of Biotechnology, Zhejiang University, Hangzhou 310058, China


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Accepted 18 March 2014.

Vitamin B6 (VB6), an essential cofactor for numerous metabolic enzymes, has recently been shown to act as a potent antioxidant and play important roles in developmental processes and stress responses. However, little is known about the possible function of VB6 in plant disease resistance response against pathogen infection. In the present study, we explored the possible involvement of VB6 in defense response against Botrytis cinerea through functional analysis of tomato VB6 biosynthetic genes. Three de novo VB6 biosynthetic genes (SlPDX1.2, SlPDX1.3, and SlPDX2) and one salvage pathway gene (SlSOS4) were identified and the SlPDX1.2, SlPDX1.3, and SlPDX2 genes were shown to encode functional enzymes involved in de novo biosynthesis of VB6, as revealed by complementation of the VB6 prototrophy in yeast snz1 and sno1 mutants. Expression of SlPDX1.2, SlPDX1.3, and SlSOS4 genes was induced by infection with B. cinerea. Virus-induced gene silencing-mediated knockdown of SlPDX1.2 or SlPDX1.3 but not SlPDX2 and SlSOS4 led to increased severity of disease caused by B. cinerea, indicating that the VB6 de novo biosynthetic pathway but not the salvage pathway is involved in tomato defense response against B. cinerea. Furthermore, the SlPDX1.2- and SlPDX1.3-silenced tomato plants exhibited reduced levels of VB6 contents and reactive oxygen species scavenging capability, increased levels of superoxide anion and H2O2 generation, and increased activity of superoxide dismutase after infection by B. cinerea. Our results suggest that VB6 and its de novo biosynthetic pathway play important roles in regulation of defense response against B. cinerea through modulating cellular antioxidant capacity.



© 2014 The American Phytopathological Society