T. Jack Morris, PhD

Distinguished Professor of Biological Sciences University of Nebraska-Lincoln School of Biological Sciences E230 Beadle Center Lincoln, NE 68588-0666 Lab Phone – 402-472-8889 Fax – 402-472-2083 Jmorris1@unl.edu

Research Interests in the Morris Lab

We study plant viruses. My lab has pioneered studies on small RNA viruses of the Family Tombusviridae. These are some of the smallest of viruses infecting eukaryotes. We have contributed to understanding fundamental aspects of virus assembly, RNA replication and the molecular basis of virus-host interactions. Most recently, we have been exploring mechanisms of host plant resistance in Arabidopsis to turnip crinkle virus (TCV) infection. The ability to manipulate both the viral pathogen and the host plant using molecular genetic and genomic tools makes our model system particularly suitable for the study of host-pathogen interactions at the molecular level. Expression of resistance genes (R genes) is one defensive strategy employed by plants to confer resistance to specific strains of a pathogen including viruses. R genes initiate a hypersensitive type of resistance cascade (HR) that limits systemic invasion of a pathogen. Post-transcriptional silencing of the invading RNAs directed against viral pathogens has been recognized as another general defense system in plants. The recent finding that many plant viruses encode proteins that suppress this anti-viral defense system suggests that co-evolutionary adaptation between plant defense and viral counter-defense strategies is an evolutionarily active process. Recent work from our lab has shown that both types of defensive strategies are employed by plants to counteract invasion by Turnip crinkle virus (TCV), a member of the small RNA virus family, Tombusviridae. Our research has shown that specific molecular interaction between TCV coat protein (CP) and an Arabidopsis transcription factor appears to be an essential step in triggering a specific R gene based HR response. We have also shown that systemic invasion of host plants by this virus is also promoted by the viral CP functioning as a suppressor of the host RNA silencing system. Our results demonstrate that multiple functions of the viral CP ensure systemic invasion by the virus and provide important clues toward understanding the relatively sophisticated network of defense pathways that protect plants against viral infections.

We are also exploring the development and application of RNA plant virus vectors for transient expression of "foreign" proteins in plants. We have successfully engineered a tobacco mosaic virus based vector to express several animal viral antigens in plants. Our most exciting result so far has been the demonstration that foot and mouth disease viral capsid proteins expressed in plants can be used to protect experimental animals from FMDV infection. In a recent collaboration with Dr. Charles Wood, we have applied the use of plant viral vectors to express specific antigens of Human Immunodeficiency Virus (HIV-1) in plant systems. Our ultimate objective is to develop an inexpensive vaccine.

Refereed Published Journal Articles since 2000:

Ren, T., Qu, F., and Morris, T.J. 2005. Turnip crinkle virus coat protein binds to and prevents the nuclear localization of an Arabidopsis NAC transcription factor. Virology 331, 316-324.

Chang Won Choi, Feng Qu, Tao Ren, Xiaohong Ye & T. Jack Morris. 2004. The RNA silencing suppressor function of Turnip crinkle virus coat protein cannot be attributed to its interaction with the Arabidopsis protein TIP. J Gen Virol 85, 3415-3420.

D. M. Pérez Filgueira, M. Mozgovoj, A. Wigdorovitz, M. J. Dus Santos, V. Parreño, K. Trono, F.M. Fernandez, C. Carrillo, T.J. Morris & M.V. Borca . 2004. Passive Protection to Bovine Rotavirus (BRV) Infection Induced by a BRV VP8* Produced in Plants Using a TMV-based Vector. Arch Virol (in press).

D. M. Pérez Filgueira, B. P. Brayfield, S. Phiri, M.V. Borca, C. Wood & T. J. Morris. 2004. Preserved antigenicity of HIV-1 p24 produced and purified in high yields from plants inoculated with a tobacco mosaic virus (TMV)-derived vector. J. Virological Methods 121, 201-208.

D. M. Pérez Filgueira, P. Zamorano, M. Domínguez , O. Taboga, P. Del Médico, A. Romera, T.J. Morris , M. V. Borca, and A. Sadir. 2003. Bovine Herpes Virus gD protein produced in plants using a recombinant TMV vector possesses authentic antigenicity. Vaccine 21, 4201-4209.

Qu, F., Ren, T., and Morris, T.J. 2003. The coat protein of turnip crinkle virus suppresses posttranscriptional gene silencing at an early initiation step. J. Virol. 77: 511-522.

Qu, F., and Morris, T.J. 2002. Efficient infection of Nicotiana benthamiana by Tomato bushy stunt virus is facilitated by the coat protein and maintained by p19 through suppression of gene silencing. MPMI 15: 193-202.

Hall, J.S., French, R., Morris, T.J. & Stenger, D.C., 2001. Structure and temporal dynamics of populations within Wheat Streak Mosaic virus isolates. J. Virol., 75: 10231-10243.

Hall, J.S., Stenger, D.C., Hein, G.L. Morris, T.J. and Stenger, D.C. 2001. Three distinct mechanisms facilitate genetic isolation of sympatric Wheat Streak Mosaic Virus lineage. Virology 282: 230-236.

Cohen, Y., F. Qu, A. Gisel, T. J. Morris and P. C. Zambryski. 2000. Nuclear Localization of Turnip Crinkle Virus Movement Protein P8. Virology 273: 276-285.

Ren, T, Qu, F., & Morris, T.J. 2000. HRT gene function requires interaction between a NAC protein and viral capsid protein to confer resistance to Turnip Crinkle Virus. Plant Cell 12:1917-1925.

Choi, I.R., Stenger, D.C., Morris, T.J. and French, R. 2000. A plant virus vector for systemic expression of foreign genes in cereals. The Plant Journal 23: 547-555.

Robertson, N. L., French, R. & Morris, T.J. 2000. The Open reading Frame 5A of Foxtail Mosaic Virus is Expressed In Vivo and is Dispensable for Systemic Infection. Arch. Virol. 145: 1685-1698.

Qu, F., and Morris, T.J. 2000. Cap-Independent translational enhancement of Turnip Crinkle Virus genomic and subgenomic RNAs. J. Virol. 74: 1085-1093.