The pathogenicity factor of DNA virus interacts with Arabidopsis deubiquitinases UBP12/13 to promote viral infection
5 affiliations
- 1Guangdong Provincial Key Laboratory of Applied Botany & Key Laboratory of National Forestry and Grassland Administration on Plant Conservation and Utilization in Southern China, South China Botanical Garden, Chinese Academy of Sciences, Guangzhou, China.
- 2Plant Protection Research Institute, Guangdong Academy of Agricultural Sciences, Key Laboratory of Green Prevention and Control on Fruits and Vegetables in South China Ministry of Agriculture and Rural Affairs, Guangdong Provincial Key Laboratory of High Technology for Plant Protection, Guangzhou, People's Republic of China.
- 3University of Chinese Academy of Sciences, Beijing, China.
- 4Temasek Life Sciences Laboratory, Singapore, Singapore.
- 5School of Applied Science, Republic Polytechnic, Singapore, Singapore.
Abstract
Plant DNA viruses, such as Cauliflower mosaic virus (CaMV) and Cabbage leaf curl virus (CaLCuV), are devastating pathogens that cause substantial yield losses in crops worldwide. These viruses assemble their genomes into minichromosomes with host histones. Histone post-translational modifications (PTMs) are important for viral replication and host resistance. In this study, we demonstrate that the CaMV pathogenicity factor P6 interacts with Arabidopsis deubiquitinases UBP12 and UBP13, which are typically negative regulators of plant immunity. Using affinity purification–mass spectrometry (AP-MS), we identified UBP12/13 as prominent P6 interactors and confirmed their nuclear association. CaMV infection and P6 overexpression increased UBP12 abundance, suggesting the latter promotes viral infection. By contrast, ubp12/13 mutants exhibited enhanced resistance, characterized by reduced accumulation of viral DNA and transcripts. Chromatin immunoprecipitation (ChIP)-qPCR showed that the monoubiquitinated H2A (H2Aub) and H3K27me3 modifications on the CaMV 35S promoter, but not the 19S promoter, were significantly elevated in ubp12/13 mutants compared with wild-type plants. Furthermore, UBP12/13 are also targeted by AC2, a transcriptional activator from CaLCuV, indicating a conserved strategy among plant DNA viruses. Our findings support a working model in which viral pathogenicity factors hijack UBP12/13, which in turn may alter H2Aub homeostasis on viral minichromosomes to relieve epigenetic silencing and promote infection. Together, these findings point to a previously unrecognized route by which plant DNA viruses may influence host chromatin-associated pathways and identify UBP12/13 as potential targets for engineering virus-resistant crops. Author summary: Plant DNA viruses, including double-stranded DNA viruses (caulimoviruses) and single-stranded DNA viruses (geminiviruses), are critical crop pathogens worldwide. Upon infection, viral genomes are packaged with host histones to form minichromosomes, and histone post-translational modifications (PTMs) on these minichromosomes play a critical role in regulating viral replication and gene expression. In this study, we identified that Arabidopsis deubiquitinases UBP12 and UBP13 are recruited by the P6 protein of CaMV might influence the epigenetic state of the 35S promoter in viral minichromosomes. We confirmed that P6 directly interacts with UBP12/13 in the nucleus, and CaMV infection and P6 overexpression specifically enhance UBP12 protein abundance. We found that ubp12/13 mutants showed enhanced resistance to CaMV and had reduced accumulation of viral DNA. In addition, the pathogenicity factor AC2 of CaLCuV also hijacks UBP12/13 to facilitate DNA virus infection. Collectively, our results illustrate that UBP12/13 act as conserved host factors exploited by viral pathogenicity proteins to promote viral infection.
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BibTeX
@article{li2026pathogenicity,
title = {{The pathogenicity factor of DNA virus interacts with Arabidopsis deubiquitinases UBP12/13 to promote viral infection}},
author = {Shun Li and Fangqin Yu and Yi Zhang and Siqi Liu and Hui-Wen Wu and Nam-Hai Chua and Shulin Deng},
journal = {PLOS Pathogens},
year = {2026},
month = oct,
doi = {10.1371/journal.ppat.1014686},
url = {https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1014686},
note = {CC BY},
}
RIS
TY - JOUR
TI - The pathogenicity factor of DNA virus interacts with Arabidopsis deubiquitinases UBP12/13 to promote viral infection
AU - Shun Li
AU - Fangqin Yu
AU - Yi Zhang
AU - Siqi Liu
AU - Hui-Wen Wu
AU - Nam-Hai Chua
AU - Shulin Deng
PY - 2026
DA - 2026/10/15
JO - PLOS Pathogens
DO - 10.1371/journal.ppat.1014686
UR - https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1014686
AB - Plant DNA viruses, such as Cauliflower mosaic virus (CaMV) and Cabbage leaf curl virus (CaLCuV), are devastating pathogens that cause substantial yield losses in crops worldwide. These viruses assemble their genomes into minichromosomes with host histones. Histone post-translational modifications (PTMs) are important for viral replication and host resistance. In this study, we demonstrate that the CaMV pathogenicity factor P6 interacts with Arabidopsis deubiquitinases UBP12 and UBP13, which are typically negative regulators of plant immunity. Using affinity purification–mass spectrometry (AP-MS), we identified UBP12/13 as prominent P6 interactors and confirmed their nuclear association. CaMV infection and P6 overexpression increased UBP12 abundance, suggesting the latter promotes viral infection. By contrast, ubp12/13 mutants exhibited enhanced resistance, characterized by reduced accumulation of viral DNA and transcripts. Chromatin immunoprecipitation (ChIP)-qPCR showed that the monoubiquitinated H2A (H2Aub) and H3K27me3 modifications on the CaMV 35S promoter, but not the 19S promoter, were significantly elevated in ubp12/13 mutants compared with wild-type plants. Furthermore, UBP12/13 are also targeted by AC2, a transcriptional activator from CaLCuV, indicating a conserved strategy among plant DNA viruses. Our findings support a working model in which viral pathogenicity factors hijack UBP12/13, which in turn may alter H2Aub homeostasis on viral minichromosomes to relieve epigenetic silencing and promote infection. Together, these findings point to a previously unrecognized route by which plant DNA viruses may influence host chromatin-associated pathways and identify UBP12/13 as potential targets for engineering virus-resistant crops. Author summary: Plant DNA viruses, including double-stranded DNA viruses (caulimoviruses) and single-stranded DNA viruses (geminiviruses), are critical crop pathogens worldwide. Upon infection, viral genomes are packaged with host histones to form minichromosomes, and histone post-translational modifications (PTMs) on these minichromosomes play a critical role in regulating viral replication and gene expression. In this study, we identified that Arabidopsis deubiquitinases UBP12 and UBP13 are recruited by the P6 protein of CaMV might influence the epigenetic state of the 35S promoter in viral minichromosomes. We confirmed that P6 directly interacts with UBP12/13 in the nucleus, and CaMV infection and P6 overexpression specifically enhance UBP12 protein abundance. We found that ubp12/13 mutants showed enhanced resistance to CaMV and had reduced accumulation of viral DNA. In addition, the pathogenicity factor AC2 of CaLCuV also hijacks UBP12/13 to facilitate DNA virus infection. Collectively, our results illustrate that UBP12/13 act as conserved host factors exploited by viral pathogenicity proteins to promote viral infection.
SN - 1553-7374
SN - 1553-7366
ER -