HighlightA satellite DNA-encoded protein (βC1) is localized in the chloroplast. The intercellular events associated with βC1-induced photosynthetic inhibition and vein clearing symptom formation are discussed.
Summary
Begomoviruses have emerged as a group of plant pathogens that cause devastating diseases in a wide range of crops in tropical and subtropical regions of the world. Betasatellites, the circular single‐stranded DNA molecules with the size of almost half of that of the associated helper begomoviruses, are often essential for the production of typical disease symptoms in several virus‐host systems. Association of betasatellites with begomoviruses results in more severe symptoms in the plants and affects the yield of numerous crops leading to huge agroeconomic losses. βC1, the only protein encoded by betasatellites, plays a multifaceted role in the successful establishment of infection. This protein counteracts the innate defence mechanisms of the host, like RNA silencing, ubiquitin‐proteasome system and defence responsive hormones. In the last two decades, the molecular aspect of betasatellite pathogenesis has attracted much attention from the researchers worldwide, and reports have shown that βC1 protein aggravates the helper begomovirus disease complex by modulating specific host factors. This review discusses the molecular aspects of the pathogenesis of betasatellites, including various βC1‐host factor interactions and their effects on the suppression of defence responses of the plants.
Summary
Geminivirus disease complexes potentially interfere with plants physiology and cause disastrous effects on a wide range of economically important crops throughout the world. Diverse geminivirus betasatellite associations exacerbate the epidemic threat for global food security. Our previous study showed that βC1, the pathogenicity determinant of geminivirus betasatellites induce symptom development by disrupting the ultrastructure and function of chloroplasts. Here we explored the betasatellite‐virus‐chloroplast interaction in the scope of viral pathogenesis as well as plant defence responses, using
Nicotiana benthamiana
—Radish leaf curl betasatellite (RaLCB) as the model system. We have shown an interaction between RaLCB‐encoded βC1 and one of the extrinsic subunit proteins of oxygen‐evolving complex of photosystem II both
in vitro
and
in vivo
. Further, we demonstrate a novel function of the
Nicotiana benthamiana
oxygen‐evolving enhancer protein 2 (PsbP), in that it binds DNA, including geminivirus DNA. Transient silencing of
PsbP
in
N. benthamiana
plants enhances pathogenicity and viral DNA accumulation. Overexpression of PsbP impedes disease development during the early phase of infection, suggesting that PsbP is involved in generation of defence response during geminivirus infection. In addition, βC1‐PsbP interaction hampers non‐specific binding of PsbP to the geminivirus DNA. Our findings suggest that betasatellite‐encoded βC1 protein accomplishes counter‐defence by physical interaction with PsbP reducing the ability of PsbP to bind geminivirus DNA to establish infection.
The compound microsatellites consist of two or more individual microsatellites, originate from mutation or imperfection in simple repeat sequences. The reports on systematic analysis of the occurrence, size and density of compound microsatellite (cSSR) types are very rare. Our study indicates that cSSRs are clustered at specific regions in the begomovirus genomes. cSSRs were overrepresented in majority of begomovirus genomes indicating that they might have some functional significance. Further, non-random distribution pattern of cSSR in begomovirus genomes was significantly correlated with the recombination breakpoint positions in the genome. The analysis of cSSR regions in the viral genome indicates the presence of stem loop (hairpin) secondary structure. The significance of these findings in biology of geminiviruses is discussed based on our present understanding of recombination and repetitive DNA. To our knowledge, this is the first analysis suggesting the possible association between recombination and microsatellites in any viral genome.
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