1.11.4S
PROGRAMMATIC FEATURES OF PLANT PARARETROVIRAL PATHOGENESIS

SN COVEY1, NS ALKAFF1, D McCALLUM1, DS TURNER1, RJ NOAD1, M KREIKE1, P DALE1, R PINDER1, A PAGE1, J MILNER2 and E CECCHINI2

1John lnnes Centre, Norwich Research Park, Colney, Norwich NR4 7UH, UK; 2Plant Molecular Science Group, Division of Biochemistry and Molecular Biology, Institute of Biomedical and Life Sciences, Glasgow University, Glasgow 12 8QQ, Scotland, UK

Background and objectives
Infection of susceptible plants by viruses usually leads to the development of systemic symptoms. Pathogenic characteristics of systemic virus infections in a wide variety of host-virus combinations often share similar features. These include common symptoms of vein-associated chlorosis, mosaics, development of dark green tissues, etc. These responses could be as a result of generalized stress caused by the pathogen competing for host resources. Alternatively, they could reflect a more organized host response involving regulated gene expression. We have been studying molecular interactions between crucifer plants and the DNA pararetrovirus cauliflower mosaic virus (CaMV) to understand how the host response to virus infection is organized. Infections by different combinations of CaMV genetic variants and crucifer species lead to pathologies with a wide variety of characteristics. These range from asymptomatic infections, elicitation of a broad range of leaf coloration effects, and host recovery phenotypes. We want to understand how specific pathogenic responses to CaMV infection relate to viral activity, and how the host regulates the virus and its own response to infection.

Results and conclusions
We have exploited a variety of approaches to address these questions. We have used genetic variation to identify host-virus combinations that result in specific types of disease characteristic and determined the consequences for specific viral functions at the molecular level. Viral variants have been obtained either from natural populations or by generating site-directed viral mutants in vitro. Infections in highly susceptible plants such as turnip (Brassica rapa) or Arabidopsis cause a wide variety of symptomatic host-response phenotypes, including production of dark green tissues, a characteristic of many plant pathogen infections. Early in infection, virus accumulates more in the dark green tissue than the chlorotic tissue, whereas dark green tissues produced late in infection have less virus than the chlorotic tissue. Infection of CaMV host plants carrying reporter genes controlled by the CaMV 35S promoter indicates that virus accumulation in symptomatic tissues is differentially regulated by the 35S promoter. The pattern of this regulation suggests that the virus is responding to a coordinated pathogenic programme of altered gene expression rather than an indirect effect of diseased tissues. This conclusion is supported by the finding that symptomatic effects can be elicited in transgenic plants expressing a viral protein in the absence of infection [1]. Infection of plants by CaMV with mutations in the 35S promoter generate altered patterns of symptoms consistent with an interaction between the host and viral transcription. In those host species (e.g. Brassica oleraceae) that show a recovery from CaMV infection, a similar early host response with programmatic features is observed but one that operates at the post-transcriptional level. This mechanism is similar to transgene-elicited post-transcriptional gene silencing [2]. Thus, plants appear to elicit organized responses from plants during compatible infections by viruses. An important question is whether such responses are fundamentally pathogenic and common to many infections, or are related to properties of plant viruses that are subject to mechanisms of gene regulation that operate primarily on the host.

References
1. Cecchini E, Gong Z, Geri C et al., 1997. Molecular Plant-Microbe Interactions 10, 1094-1101.
2. Covey SN, AI-Kaff NS, Langara A, Turner DS, 1997. Nature 385, 781-782.