4.5 Article

Diverse begomovirus-betasatellite complexes cause tomato leaf curl disease in the western India

Journal

VIRUS RESEARCH
Volume 328, Issue -, Pages -

Publisher

ELSEVIER
DOI: 10.1016/j.virusres.2023.199079

Keywords

Detection; Geminivirus; Infection; Leaf curl; Pathogenesis; Recombination; Resistance; Satellite; Vegetable

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In the western part of India, a study on the characterization of virus complexes with tomato leaf curl disease (ToLCD) caused by begomoviruses was conducted. A complex of 19 DNA-A and 4 DNA-B begomoviruses as well as 15 betasatellites associated with ToLCD was identified. The study also discovered a novel betasatellite and an alphasatellite, and detected recombination breakpoints in the cloned begomoviruses and betasatellites. The findings suggest the potential of these virus complexes in breaking disease resistance and expanding their host range, highlighting the need to investigate the interaction mechanism between resistance-breaking virus complexes and infected hosts.
In the Indian sub-continent, tomato leaf curl disease (ToLCD) of tomato caused by begomoviruses has emerged as a major limiting factor for tomato cultivation. Despite the spread of this disease in the western India, a systematic study on the characterization of virus complexes with ToLCD is lacking. Here, we report the identification of a complex of begomoviruses including 19 DNA-A and 4 DNA-B as well as 15 betasatellites with ToLCD in the western part of the country. Additionally, a novel betasatellite and an alphasatellite were also identified. The recombination breakpoints were detected in the cloned begomoviruses and betasatellites. The cloned infectious DNA constructs cause disease on the tomato (a moderately virus-resistant cultivar) plants, thus fulfilling Koch's postulates for these virus complexes. Further, the role of non-cognate DNA B/betasatellite with ToLCD-associated begomoviruses on disease development was demonstrated. It also emphasizes the evolutionary potential of these virus complexes in breaking disease resistance and plausible expansion of its host range. This necessitates to investigate the mechanism of the interaction between resistance breaking virus complexes and the infected host.

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