Research Article: Cultivated Grapevines Represent a Symptomless Reservoir for the Transmission of Hop Stunt Viroid to Hop Crops: 15 Years of Evolutionary Analysis

Date Published: December 24, 2009

Publisher: Public Library of Science

Author(s): Yoko Kawaguchi-Ito, Shi-Fang Li, Masaya Tagawa, Hiroyuki Araki, Masafumi Goshono, Shingen Yamamoto, Mayumi Tanaka, Masako Narita, Kazuaki Tanaka, Sheng-Xue Liu, Eishiro Shikata, Teruo Sano, Ding Xiang Liu. http://doi.org/10.1371/journal.pone.0008386

Abstract: Hop stunt was a mysterious disorder that first emerged in the 1940s in commercial hops in Japan. To investigate the origin of this disorder, we infected hops with natural Hop stunt viroid (HpSVd) isolates derived from four host species (hop, grapevine, plum and citrus), which except for hop represent possible sources of the ancestral viroid. These plants were maintained for 15 years, then analyzed the HpSVd variants present. Here we show that the variant originally found in cultivated grapevines gave rise to various combinations of mutations at positions 25, 26, 54, 193, and 281. However, upon prolonged infection, these variants underwent convergent evolution resulting in a limited number of adapted mutants. Some of them showed nucleotide sequences identical to those currently responsible for hop stunt epidemics in commercial hops in Japan, China, and the United States. Therefore, these results indicate that we have successfully reproduced the original process by which a natural HpSVd variant naturally introduced into cultivated hops was able to mutate into the HpSVd variants that are currently present in commercial hops. Furthermore, and importantly, we have identified cultivated grapevines as a symptomless reservoir in which HSVd can evolve and be transmitted to hop crops to cause epidemics.

Partial Text: Viroids are the smallest known pathogens and cause severe to mild diseases in economically important crop species [1]. They are single-stranded, circular, and self-replicating non-coding RNAs, with the size ranging ∼250–400 nucleotides. Viroid replication is dependent on host transcriptional machinery, and pathogenicity depends entirely on interactions with cellular components of the host [2]–[7]. The small size and unique molecular structure of viroid genomes makes them an attractive system to analyze molecular features responsible for pathogenesis [8]–[14], RNA transport [15]–[18], or molecular evolution and adaptation to specific host species [19]–[26].

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http://doi.org/10.1371/journal.pone.0008386

 

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