Nicotiana benthamiana anti-silencing function-1 mediated chromatin modulation during geminivirus infection.

Histones are rapidly loaded onto the geminivirus genome upon entry into plant cells leading to the formation of a eukaryotic chromatin-like structure "minichromosome" that supports its replication and transcription but the underlying mechanism behind this process has not been fully defined. From a host-virus perspective, histone chaperones, a crucial component in regulating chromatin architecture are recognized as a potential determinant in animal virus infection and are well studied, but their possible involvement in plant virus pathogenesis has been unexplored. ASF1, a pivotal histone chaperone facilitates the deposition of histone H3 and H4 onto DNA, which is necessary for the formation of eukaryotic chromatin. Here, we report that overexpression of specific histone chaperones (HCs) NbASF1A and NbASF1B genes facilitate the deposition of histone onto incoming virus DNA preventing its accessibility for both DNA synthesis and transcription machinery and this approach efficiently limits the development of geminivirus related disease symptoms progression. Conversely, the knockdown of both NbASF1A and NbASF1B enhances virus accumulation and disease progression and this process is supported by the Radiation sensitive protein 51 (RAD51) of Homologous recombination repair (HRR) pathway. This study presents a novel finding about HCs NbASF1A and NbASF1B conferring robust antiviral defence against geminiviruses. Supplementary Information: The online version contains supplementary material available at 10.1007/s12298-025-01580-8.