Silicon modulates expression of pathogen defense-related genes during alleviation of copper toxicity in Nicotiana tabacum

Abstract

Plants treated with metals better fend off infection by pathogens. This activity is mediated, at least in part, by the activation of the salicylic acid (SA) signaling pathway. Previous work in our laboratory demonstrated that silicon (Si) could alleviate copper (Cu) toxicity stress in Nicotiana tabacum. However, how Si affected expression of genes involved in SA biosynthesis and signaling in N. tabacum under Cu stress was unclear. Therefore, we investigated this at two time points. Roots of plants treated with Cu toxicity for one week exhibited increased transcript levels for Isochorismate Synthase1, a gene encoding a key enzyme involved in SA biosynthesis and the addition of Si further enhanced expression. Microarray analysis identified a number of disease defense-associated genes up-regulated in N. tabacum roots after one week of Cu toxicity treatment and further increased when plants were also supplemented with Si. However, the effect of Si on expression of these genes was lost after three weeks of treatment, indicating these effects are dynamic.

Keywords:

• Cu
• metal toxicity
• PR-protein
• salicylic acid
• Si
• tobacco

Acknowledgments

The authors thank MOgene, St. Louis, MO, for performing the microarray analysis. The authors also thank Wendy Zellner (Department of Biological Sciences, University of Toledo) for her assistance with the manuscript and the University of Toledo Plant Science Research Center. Mention of trade names or commercial products in this publication is solely for the purpose of providing specific information and does not imply recommendation or endorsement by the University of Toledo or the U.S. Department of Agriculture. USDA is an equal opportunity provider and employer.

Conflict of interest

No conflict of interest was reported by the authors.

Additional information

Funding

This work was supported in part by US Department of Agriculture-Agricultural Research Service Specific Cooperative Agreement (grant number: 58-5082-6-012).