Nucleotide and amino acid variation in the coat protein coding region of turnip mosaic virus isolates and possible involvement in the interaction with the brassica resistance geneTuRB01

The nucleotide and predicted amino acid sequences of the coat protein coding region of four isolates (UK 1, CZE 1, CDN 1 and GK 1) and a putative mutant of one of these isolates (UK 1M) of turnip mosaic virus (TuMV) were determined. Comparisons between these and those of previously sequenced isolates showed homologies of 88.6–99.9% in nucleotides and 93.4–100% in amino acid sequences. Nucleotide substitutions were revealed at 180 different positions that give rise to 30 predicted amino acid changes. The coat protein coding regions consisted of 864 nucleotides, with the exception of GK 1 which had 861, having a deletion in amino acid position 44. This is the first recorded deletion in the coat protein coding region of TuMV. Alignment of the predicted amino acid sequences of UK 1, CZE 1, CDN 1 and GK 1 isolates with the previously sequenced CDN 2, CHN, JPN 1, JPN 2, JPN (31), L12396 and KOR isolates revealed three distinct groups which, with a few exceptions, were correlated with the geographical and/or host plant origin of isolates. The GK 1 isolate showed the lowest nucleotide (88.6–89.9%) and amino acid (93.4–96.2%) homologies with the other isolates, whereas the UK 1 isolate showed the highest nucleotide homology (89.7–99.9%) and CDN 1 showed the highest amino acid homology (95.9–99%). The coat protein coding region of the putative mutant isolate (UK 1M) had a single nucleotide difference (G to A) from UK 1 at position 9 which did not give rise to any change in the predicted amino acid sequence. UK 1M is able to infect Brassica napus plants possessing a mapped resistance gene ( TuRB01 ) that is effective against UK 1. The phenotypes of most of the sequenced isolates on plants containing TuRB01 are known, and these are consistent with the hypothesis that the single nucleotide substitution at position 9 of the coat protein coding region conditions the interaction with this gene. All isolates tested that had the residue G 9 gave no detectable replication in plants possessing TuRB01 , whereas isolates that had the residue A 9 were either partially virulent on plants carrying TuRB01 causing local infection only, or were fully virulent resulting in full systemic infection. This hypothesis is unprecedented in plant virus interactions and further experimentation utilizing full-length infectious clones of TuMV will be necessary to test its validity.