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.

Chilli, which encompasses several species in the genus Capsicum, is widely consumed throughout the world. In the Indian subcontinent, production of chilli is constrained due to chilli leaf curl disease (ChiLCD) caused by begomoviruses. Despite the considerable economic consequences of ChiLCD on chilli cultivation in India, there have been scant studies of the genetic diversity and structure of the begomoviruses that cause this disease. Here we report on a comprehensive survey across major chilli-growing regions in India. Analysis of samples collected in the survey indicates that ChiLCD-infected plants are associated with a complex of begomoviruses (including one previously unreported species) with a diverse group of betasatellites found in crops and weeds. The associated betasatellites neither enhanced the accumulation of the begomovirus components nor reduced the incubation period in Nicotiana benthamiana. The ChiLCD-associated begomoviruses induced mild symptoms on Capsicum spp., but both the level of helper virus that accumulated and the severity of symptoms were increased in the presence of cognate betasatellites. Interestingly, most of the begomoviruses were found to be intra-species recombinants. The betasatellites possess high nucleotide variability, and recombination among them was also evident. The nucleotide substitution rates were determined for the AV1 gene of begomoviruses (2.60610 23 substitutions site 21 year 21 ) and the bC1 gene of betasatellites [chilli leaf curl betasatellite (ChiLCB), 2.57610 24 substitution site 21 year 21 ; tomato leaf curl Bangladesh betasatellite (ToLCBDB), 5.22610 24 substitution site 21 year 21 ]. This study underscores the current understanding of Indian ChiLCD-associated begomoviruses and also demonstrates the crucial role of betasatellites in severe disease development in Capsicum spp.

Chilli (Capsicum sp.) is one of the economically important spice and vegetable crops grown in India and suffers great losses due to the infection of begomoviruses. Conventional breeding approaches have resulted in development of a few cultivars of chilli resistant to begomoviruses. A severe leaf curl disease was observed on one such resistant chilli cultivar (Capsicum annuum cv. Kalyanpur Chanchal) grown in the experimental field of the Jawaharlal Nehru University, New Delhi. Four different viral genomic components namely, Chilli leaf curl virus (DNA A), Tomato leaf curl Bangladesh betasatellite (DNA β), Tomato leaf curl New Delhi virus (DNA A), and Tomato leaf curl Gujarat virus (DNA B) were associated with the severe leaf curl disease. Further, frequent association of these four genomic components was also observed in symptomatic plants of other chilli cultivars (Capsicum annuum cv. Kashi Anmol and Capsicum chinense cv. Bhut Jolokia) grown in the experimental field. Interaction studies among the isolated viral components revealed that Nicotiana benthamiana and chilli plants inoculated with four genomic components of begomoviruses exhibited severe leaf curl disease symptoms. In addition, this synergistic interaction resulted in increased viral DNA accumulation in infected plants. Resistant chilli plants co-inoculated with four genomic components of begomoviruses showed drastic reduction of host basal (ascorbate peroxidase, thionin, polyphenol oxidase) and specific defense-related gene (NBS-LRR) expression. Our results suggested that synergistic interaction among begomoviruses created permissive cellular environment in the resistant chilli plants which leads to breakdown of natural resistance, a phenomenon observed for the first time in chilli.

Summary Autophagy is a conserved self‐cleaning and renewal system required for cellular homeostasis and stress tolerance. Autophagic processes are also implicated in the response to ‘non‐self’ such as viral pathogens, yet the functions and mechanisms of autophagy during plant virus infection have only recently started to be revealed. Compelling evidence now indicates that autophagy is an integral part of antiviral immunity in plants. It can promote the hypersensitive cell death response upon incompatible viral infections or mediate the selective elimination of entire particles and individual proteins from compatible viruses in a pathway similar to xenophagy in animals. Several viruses, however, have evolved measures to antagonize xenophagic degradation or utilize autophagy to suppress disease‐associated cell death and other defence pathways like RNA silencing. Here, we highlight the current advances and gaps in our understanding of the complex autophagy–virus interplay and its consequences for host immunity and viral pathogenesis in plants.

Geminiviruses constitute a group of plant viruses, with a ssDNA genome, whose replication in the nucleus of an infected cell requires the function of geminivirus-encoded replication initiator protein (Rep). Our results suggest that monoubiquitinated histone 2B (H2B-ub) promotes tri-methylation of histone 3 at lysine 4 (H3-K4me3) on the promoter of Chilli leaf curl virus (ChiLCV). We isolated homologues of two major components of the monoubiquitination machinery: UBIQUITIN-CONJUGATING ENZYME2 (NbUBC2) and HISTONE MONOUBIQUITINATION1 (NbHUB1) from N. benthamiana. ChiLCV failed to cause disease in NbUBC2-, and NbHUB1-silenced plants, at the same time, H2B-ub and H3-K4me3 modifications were decreased, and the occupancy of RNA polymerase II on the viral promoter was reduced as well. In further investigations, Rep protein of ChiLCV was found to re-localize NbUBC2 from the cytoplasm to the nucleoplasm, like NbHUB1, the cognate partner of NbUBC2. Rep was observed to interact and co-localize with NbHUB1 and NbUBC2 in the nuclei of the infected cells. In summary, the current study reveals that the ChiLCV Rep protein binds the viral genome and interacts with NbUBC2 and NbHUB1 for the monoubiquitination of histone 2B that subsequently promotes trimethylation of histone 3 at lysine 4 on ChiLCV mini-chromosomes and enhances transcription of the viral genes.