Viroid territorial behavior: a likely effect of population bottleneks during host colonization
Abstract
Viroids, like RNA viruses, propagate in their hosts as populations of closely-related sequence variants (quasi-species). When assayed individually, such variants often incite distinct phenotypes but their stability along time may vary because viroids, like chrysanthemum chlorotic mottle viroid (CChMVd), display a hight mutation rate [2] that rapidly generates heterogeneous populations. The behavior of these populations is essentially determined by interference among individual components, which in viroids must occur at the RNA level. During host colonization virus populations suffer bottlenecks imposed by the host, the vector, and the territorial behavior (superinfection exclusion) of the infecting viruses, which limit the number of genomes entering and replicating in individual cells [3]. Some reports suggest that bottlenecks also operate during viroid infection, but such issue has not been further addressed. Here we have examined the evolution in time and space of two natural CChMVd variants: one containing a UUUC tetraloop strictly associated with symptoms and the other with a GAAA tetraloop and asymptomatic [1]. Inoculation with the latter induced no phenotype, with only variants with the same tetraloop in the progeny analyzed by RT-PCR, cloning and sequencing. Conversely, early symptoms incited by the first variant consisted in chlorotic and green sectors. RT-PCR, cloning and sequencing of the progeny, and deep sequencing of the viroid-derived RNAs generated by RNA silencing, showed that variants with the UUUC tetraloop predominate in chlorotic sectors, while they coexist in green sectors with others having one or two mutations in the pathogenic determinant. Cloning and bioassay of these mutant variants resulted in asymptomatic infections (with the UUUC tetraloop absent in the progeny), showing that a single substitution in the tetraloop annuls pathogenicity, a finding consistent with involvement of an RNA silencing mechanism. Therefore, pathogenic and non-pathogenic CChMVd variants exhibit distinct evolutionary patterns. The very high mutation rate of CChMVd, combined with the ability of different variants to preferentially colonize some leaf sectors and exclude other variants, may account for the observed results.
Autore Pugliese
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Serra P.; Navarro B.; Di Serio F.; Flores R.
Titolo volume/Rivista
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Anno di pubblicazione
2015
ISSN
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ISBN
978-3-95758-006-1
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Settori ERC
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