The chloroplast is one of the most dynamic organelles of a plant cell. It carries out photosynthesis, synthesizes major phytohormones, plays an active part in the defence response and is crucial for interorganelle signalling. Viruses, on the other hand, are extremely strategic in manipulating the internal environment of the host cell. The chloroplast, a prime target for viruses, undergoes enormous structural and functional damage during viral infection. Indeed, large proportions of affected gene products in a virus-infected plant are closely associated with the chloroplast and the process of photosynthesis. Although the chloroplast is deficient in gene silencing machinery, it elicits the effector-triggered immune response against viral pathogens. Virus infection induces the organelle to produce an extensive network of stromules which are involved in both viral propagation and antiviral defence. From studies over the last few decades, the involvement of the chloroplast in the regulation of plant-virus interaction has become increasingly evident. This review presents an exhaustive account of these facts, with their implications for pathogenicity. We have attempted to highlight the intricacies of chloroplast-virus interactions and to explain the existing gaps in our current knowledge, which will enable virologists to utilize chloroplast genome-based antiviral resistance in economically important crops.
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.
Background Geminiviruses are circular, single-stranded viruses responsible for enormous crop loss worldwide. Rapid expansion of geminivirus diversity outweighs the continuous effort to control its spread. Geminiviruses channelize the host cell machinery in their favour by manipulating the gene expression, cell signalling, protein turnover, and metabolic reprogramming of plants. As a response to viral infection, plants have evolved to deploy various strategies to subvert the virus invasion and reinstate cellular homeostasis. Main body Numerous reports exploring various aspects of plant-geminivirus interaction portray the subtlety and flexibility of the host–pathogen dynamics. To leverage this pool of knowledge towards raising antiviral resistance in host plants, a comprehensive account of plant’s defence response against geminiviruses is required. This review discusses the current knowledge of plant’s antiviral responses exerted to geminivirus in the light of resistance mechanisms and the innate genetic factors contributing to the defence. We have revisited the defence pathways involving transcriptional and post-transcriptional gene silencing, ubiquitin-proteasomal degradation pathway, protein kinase signalling cascades, autophagy, and hypersensitive responses. In addition, geminivirus-induced phytohormonal fluctuations, the subsequent alterations in primary and secondary metabolites, and their impact on pathogenesis along with the recent advancements of CRISPR-Cas9 technique in generating the geminivirus resistance in plants have been discussed. Conclusions Considering the rapid development in the field of plant-virus interaction, this review provides a timely and comprehensive account of molecular nuances that define the course of geminivirus infection and can be exploited in generating virus-resistant plants to control global agricultural damage.
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