1.11.68
POTYVIRUS-POTATO PLANT INTERACTIONS: A CASE STUDY ON POTATO VIRUS

JPT VALKONEN1,2, A MERITS2, T KEKARAINEN1, U PUURAND2, JH HAMALAINEN1, J ANDREJEVA2, M RAJAMAKI1,2, I ORUECHEVARRIA1, JF KREUZE1, VA SORRI1, KN WATANABE3 and M SARMA2

1Dept. Plant Biology, Genetic Centre, Swedish University of Agricultural Sciences (SLU), PO Box 7080, S-75007 Uppsala, Sweden; 2Institute of Biotechnology, Viikki Biocentre 1, PO Box 56, FIN-00014 University of Helsinki, Finland; 3Dept. Biotechnological Science, Kinki University, Wakayama, 649-64, Japan.

Background and objectives
Potato A potyvirus (PVA) (family Potyviridae) is widespread in potato production areas in the Northern hemisphere and can reduce potato yields by up to 40%. It is one of the most important potato viruses, but it is relatively little studied compared to other potato-infecting viruses such as potato Y potyvirus, potato X potexvirus and potato leaf roll luteovirus. The aim of our studies is to characterize the molecular and biological variability of PVA and relate the biological variability with genetical differences among strains of PVA. This is possible using a full-length, infectious cDNA clone (icDNA) of PVA [1] as a target of directed mutagenesis and gene exchange. Our main goal is to identify the gene(s) of PVA that specifically activate resistance genes in potato. In order to understand how potato resistance genes recognize PVA, genetic mapping was carried out for localization and isolation of a PVA resistance gene in potato.

Results and conclusions
Examination of 21 isolates of PVA [2] has shown that they can be grouped into four strain groups based on the four types of responses induced in potato cv. King Edward: systemic spread and induction of necrotic lesions (group 1), mottle symptoms without necrosis (group 2) or yellowing and stunting (group 4), or lack of systemic spread (group 3). These differences are at least partially related to interactions with the hypersensitive resistance gene Na(+1/-2) in King Edward, but they were not correlated with amino acid sequence differences found in the helper component-proteinase (identity 94.8%) or coat protein sequences (identity 92.9%) [2]. Amino acid substitution and gene exchange experiments carried out on the PVA icDNA clone were consistent in that these two proteins are probably not responsible for the above-mentioned different responses (unpublished). Recently, the entire nucleotide sequence was determined in six distinct strains of PVA, and some amino acid substitutions found in other proteins seem to correlate with the differential responses these strains induce in King Edward (unpublished).

In a diploid potato population under investigation, extreme resistance (ER) to PVA is expressed as no symptoms and detectable infection, but in some genotypes a necrotic reaction is observed. This resistance is derived from Solanum tuberosum subsp. andigena and is controlled by the dominant gene Ra. We have localized Ra to chromosome Xl ca. 6.8 cM distal from the gene Ry controlling ER to potato virus Y. Construction of a genomic library and screening of an expression library are ongoing to identify Ra and Ry.

References
1. Puurand U, Valkonen JPT, Makkinen K et al., 1996. Virus Research 40, 135-140.
2. Rajamski M, Merits A, Rabenstein F et al., 1998. Phytopathology 88, in press.
3. Hamalinen JH, Sorri VA, Watanabe KN et al., 1998. Theoretical and Applied Genetics 95, in press.