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Biological Sciences Department Faculty
Ph.D. Purdue University 1989
Our laboratory studies virus-host interactions. Viruses are serious agents of disease and it is critical to design new methods to combat these pathogens. We study plant viruses because they are useful model systems for examining host-pathogen interactions. Plants contain specific genes that provide resistance to viruses while the pathogen harbors genes that overcome this protection.
Our laboratory studies the interplay between virus and host genes influencing resistance to obtain a better picture of how plants protect themselves against disease. We are also examining the interactions between different virus genes to determine their role in the infection process.
My laboratory studies viruses, in particular plant viruses. Plant viruses are good tools to study for several reasons. First, plant viruses are a serious problem for several crops throughout the world. Therefore, it is essential to develop strategies to protect crop plants against these pathogens. Second, plant viruses are unable to infect humans so they are safe to work with. Third, it is somewhat easier to study virus distribution within plants than in animals. This is because the plants are structurally more simple than animals. Finally, plant viruses are similar to animal viruses. Therefore if we can understand how to combat plant viruses, it may be possible to apply these same techniques to prevent animal and human virus infections.
Interestingly, plants use different mechanisms for combating viruses than animals do. The processes by which plants protect themselves against virus infection are poorly understood, which is an important area of interest for my laboratory. Resistance of plants to viruses can also be mediated in other ways as well. For example, plant viruses can antagonize each other and this is a research area that we are pursuing. A third major focus of my laboratory is to develop an understanding of how the various viral proteins function. Each of these research areas is described in more detail below.
1)Many plants prevent virus infection by way of specific resistance genes. These genes recognize a virus and then turn on a defense response. An understanding of how this functions is still in its infancy. We have identified two different varieties of plants that are resistant to our virus. We have also discovered two different viral isolates that are able to overcome resistance in each case. We are in the process of exchanging genes between a virus that is able to overcome a specific resistance gene with a virus that does not, to identify the resistance-breaking gene. This will allow us to identify the viral gene recognized by the resistance gene and to find host factors interacting with this viral gene. In one case, we have identified the region of a viral gene responsible for breaking resistance. We are currently analyzing this region to identify the critical nucleotide sequence differences responsible for breaking resistance. This type of analysis will allow us to gain a greater understanding of how plant virus resistance works.
2)Inoculation of a host with a virus often protects that host against other isolates of the same virus. This phenomenon has been observed in both animals and in plants. The plant version is called cross protection. We have discovered that inoculation with the first virus (which we call the protecting virus) prevents the spread of the second (challenge) virus through the plant. We are currently investigating how this inhibition of spread is accomplished.
3)In many cases, viral proteins must either self-associate or bind to other viral proteins for infection to take place. We are studying these protein-protein interactions to gain new insights into how viruses cause an infection. We have focused this research in two directions: One, to determine which viral proteins interact with with which others; and two, to identify the regions of those viral proteins involved in the interactions. Thus far, we have identified several viral protein-protein interactions, some involved in self-association, others involved in binding to other proteins. This is not as difficult as it may seem since the virus that we work with has a relatively small genome and encodes only seven proteins. We are now examining these proteins to identify the portions involved in protein-protein interaction. This research will lead to new strategies for controlling virus infections.
Khandekar, S. and S. Leisner. Soluble Silicon Enhances Expression Of Arabidopsis thaliana Genes Involved In Copper Stress. Journal of Plant Physiology. 2011. 168:699-705.
Raikhy, G., Krause, C., and S. Leisner. The Dahlia mosaic virus gene VI product N-terminal region is involved in self-association. Virus Research. 2011. 159:69-72.
Zellner, W., Frantz, J., and S. Leisner. Silicon delays Tobacco ringspot virus systemic symptoms in Nicotiana tabacum. Journal of Plant Physiology. 2011. 168:1866-1869.
He, J., Gray, J., and S. Leisner. A Pelargonium ARGONAUTE4 Gene Shows Organ-Specific Expression And Differences In RNA And Protein Levels. Journal of Plant Physiology. 2010. 167: 319-325.
Khandekar, S., He, J., and S. Leisner. Complete Nucleotide Sequence Of The Toledo Isolate Of Turnip ringspot virus. Archives of Virology. 2009. 154: 1917-1922.
Hapiak, M., Li., Y., Agama, K., Swade, S., Okenka, G., Falk, J., Khandekar, S., Raikhy, G., Anderson, A., Pollock, J., Zellner, W., Schoelz, J., and S. M. Leisner. Cauliflower mosaic virus gene VI Product N-Terminus Contains Regions Involved In Resistance-Breakage, Self-Association And Interactions With Movement Protein. Virus Research. 2008. 138: 119-129.
Li, J., Frantz, J., and S. Leisner. Alleviation of Copper Toxicity In Arabidopsis thaliana By Silicon Addition To Hydroponic Solutions. Journal of the American Society of Horticultural Science. 2008. 133: 1-8.
Rajakaruna, P., Khandekar, S., Meulia, T., and S.M. Leisner. Identification And Host Relations Of Turnip Ringspot Virus, A Novel Comovirus From Ohio. Plant Disease. 2007. 91: 1212-1220.
Agama, K., S. Beach, J. Schoelz, and S.M. Leisner. The 5' third of Cauliflower mosaic virus gene VI conditions resistance-breakage in Arabidopsis ecotype Tsu-0, Phytopathology. 2002. 92: 92-96
Leisner, S.M and D. Neher. Codon composition may indicate a two domain structure for the Cauliflower mosaic virus genome. Journal of Theoretical Biology, 2002. 217: 195-201.
Li, Y., and S.M. Leisner. Multiple domains within the Cauliflower mosaic virus gene VI product interact with the full-length protein. Mol. Plant-Microbe Interact., 2002. 15: 1050-1057.
Leisner, S. M. 1999. Molecular basis of virus transport in plants, p. 161-182. In C. L. Mandahar (ed.), Molecular biology of plant viruses. Kluwer Academic Publishers, Norwell, MA.
Tang, W. and S. Leisner. Methylation of nonintegrated multiple copy DNA in plants. Biochemical and Biophysical Research Communications. 1998. 245: 403-406. Abstract
Bobish, J.J. and S. Leisner. Novel use of polA bacteria for inserting DNA fragments into Agrobacterium binary vectors. Journal of Microbiological Methods. 1997. 31: 89-94. Abstract
Tang, W. and Leisner, S. M. Cauliflower mosaic virus isolate NY8153 breaks resistance in Arabidopsis ecotype En-2. Phytopathology 87(8). 1997. 792-798. Abstract
Leisner, S. M., Turgeon, R. and Howell, S. H. effects of host plant development and genetic determinants on the long-distance movement of cauliflower mosaic virus in arabidopsis. Plant Cell 5 (2). 1993. 191-202. Abstract
Dominov, J. A. Stenzler L. Lee S. Schwarz J J. Leisner S. Howell S H. cytokinins and auxins control the expression of a gene
in nicotiana-plumbaginifolia cells by feedback regulation. Plant Cell 4 (4). 1992. 451-461. Abstract
Leisner, S.M. and S.H. Howell. Long-distance movement of plant viruses. Trends Microbiol. 1993. 1: 314-317. Abstract
Leisner, S.M. and R.Turgeon. Movement of virus and photoassimilate in the phloem: a comparative analysis. BioEssays. 1993. 15: 741-48. Abstract