Viruses as triggers of DNA rearrangements in host plants

Abstract

Andronic, L. 2012. Viruses as triggers of DNA rearrangements in host plants. Can. J. Plant Sci. 92: 1083–1091. Assessment of microsporogenesis in tomato (Lycopersicon esculentum, cultivars Fachel, Nistru and Prizior) infected with tomato aspermy virus or potato virus X and barley (Hordeum vulgare L., cultivars Galactic, Sonor, Unirea) infected with barley stripe mosaic virus showed deviations in the conjugation of homologous chromosomes and segregation of genetic material, expressed in the disruption of chromatin cohesion between homologous chromosomes. The evidence of meiotic division in targeted genotypes indicates the effect of viral infection on chiasmata number and position, promoting the redistribution of chiasmata. On the basis of cytological study, significant changes and the induction of additional exchanges offset by asynapsis were established in early diakinesis. Different parameters, determined at particular stages of meiosis, such as chromosome aberration and the mean percentage of abnormal pollen mother cells, served as cytogenetic evaluation of microsporogenesis in virus-infected tomato or barley cultivars. The study of meiotic stability in anaphase and telophase I and II revealed a significant increase in different types of abnormalities: elimination or/and lagging chromosomes, formation of chromosome and chromatid bridges with or without fragments. Reviewed examples provide data regarding genetic rearrangements in host plants as a response to viral infection.

Infection elevates diversity

“…Previous work has demonstrated that pathogens increase recombination in plants during meiotic and somatic (non-gamete) division [7][8][9] . That the few existing examples of this phenomenon span plants and animals suggests that pathogen-induced increases in the recombinant fraction could be widespread, although perhaps achieved through different means, for example transmission distortion in flies but higher recombination in plants.…”

No Evidence that Infection Alters Global Recombination Rate in House Mice

“…Theoretical models indicate that increased genetic mixing via recombination can allow organisms to more rapidly evolve to shifting parasitic pressures in their environment, a consideration that may pose a major evolutionary advantage to sex and recombination [ 48 – 50 ]. Indeed, sex and meiotic recombination have been shown to evolve [ 51 – 53 ] and plastically increase [ 54 – 56 ] in response to pathogen pressures in species with facultative sexual reproduction. However, evidence that pathogen pressures can trigger increases in meiotic recombination rates in host species with obligate sexual reproduction is currently limited to Drosophila [ 57 ].…”

Experimental evolution across different thermal regimes yields genetic divergence in recombination fraction but no divergence in temperature associated plastic recombination

“…). Similarly, exposure to parasites has been associated with elevated recombination rates (Andronic ; Singh et al. ), and nutrient stress is associated with increased recombination rates in yeast (Abdullah and Borts ) and Drosophila (Neel ).…”

“…For instance, social stress has been associated with increased recombination rates in mice (Belyaev and Borodin 1982), and temperature is known to affect rates of crossing-over in Drosophila (Plough 1917(Plough , 1921Stern 1926;Smith 1936;Grushko et al 1991). Similarly, exposure to parasites has been associated with elevated recombination rates (Andronic 2012;Singh et al 2015), and nutrient stress is associated with increased recombination rates in yeast (Abdullah and Borts 2001) and Drosophila (Neel 1941). Further, a clear link between maternal age and recombination rate has been found in humans (e.g., Kong et al 2004;Hussin et al 2011), mice (Henderson andEdwards 1968;Luthardt et al 1973) and Drosophila (Stern 1926;Bridges 1927;Redfield 1964;Lake 1984;Chadov et al 2000;Priest et al 2007;Tedman-Aucoin and Agrawal 2012;Hunter et al 2016b).…”