Research Projects

Begomovirus-associated diseases involve a diverse array of extrachromosomal circular DNA (eccDNA) elements, including deltasatellites (~0.6 kb), betasatellites, and alphasatellites . These satellites, although dependent on helper viruses for replication, often lack sequence homology with them, highlighting the dynamic nature of viral-associated DNA. Notably, infections by Ageratum yellow vein virus (AYVV) often involve recombinant DNA molecules containing sequences from both viral DNA-A and betasatellites, suggesting that begomoviral infections create a recombinogenic environment conducive to generating novel genetic elements. Among these satellites, betasatellites function as key pathogenicity determinants, significantly contributing to symptom induction. Alphasatellites, despite their autonomous replication and RNA silencing suppressor activity, show variable influence on disease development. Co-inoculation of alphasatellites with betasatellites in AYVV infections has been shown to reduce symptom severity and viral DNA accumulation, likely due to competition for replication resources. In contrast, deltasatellites show limited impact on symptom enhancement in Tomato leaf curl virus (ToLCV) infections. Additionally, some bipartite begomoviruses associate with defective DNA molecules derived from their DNA-B components, further increasing genomic complexity. Emerging studies suggest that host-derived eccDNAs also influence begomovirus infections. For example, SEGS-1, an episomal DNA in cassava, enhances cassava mosaic disease (CMD) symptoms and overcomes resistance. Similarly, in Arabidopsis thaliana, SEGS-1 co-inoculation with African cassava mosaic virus (ACMV) leads to more severe disease symptoms. These findings indicate that endogenous eccDNAs may modulate viral infection outcomes and contribute to viral evolution. Advances in next-generation sequencing (NGS) and bioinformatics have revealed eccDNAs as important components in genome plasticity and disease dynamics. In plants, eccDNAs originate from organelles and genomic repeats, such as centromeres, telomeres, rDNA, transposons, and LTR retrotransposons. Their biogenesis involves mechanisms like breakage–fusion–bridge cycles, chromothripsis, episome formation, and deletion-amplification events, mediated by homologous recombination, non-homologous end joining, replication errors, and R-loop formation. While the role of eccDNA in viral infections is still underexplored, viruses may actively induce eccDNA formation to manipulate host genome structure, facilitate viral persistence, and modulate host-virus interactions. Such manipulation may not be incidental but an evolved viral strategy. In this context, we propose that the geminiviral Rep protein may trigger eccDNA formation if two or more nonanucleotide motifs exist within the same plant chromosome. Since begomoviruses are known to interfere with host DNA methylation, they may create a permissive environment for genome instability and eccDNA generation. Additionally, viral proteins AC2/C2 and AC4/C4, due to their structural plasticity, may interact with host DNA-modifying enzymes, while the DNase-active C1 protein encoded by betasatellites could fragment host DNA, further enhancing eccDNA biogenesis. These insights suggest a deeper interplay between viral components and host genome structure, where begomoviruses might exploit eccDNA not only as a consequence of infection but as a tool for adaptation, evolution, and pathogenesis. This emerging view highlights the necessity for continued surveillance and molecular characterization of novel eccDNAs in virus-infected plants.