Suppression of Methylation-Mediated Transcriptional Gene Silencing by βC1-SAHH Protein Interaction during Geminivirus-Betasatellite Infection

PLoS Pathogens

Jamie N. Wolf¹  David M. Bisaro¹  Priya Raja¹  Sizhun Li¹  Xueping Zhou²  Xiuling Yang²  Yan Xie²  Qingtang Shen² 

[1] Department of Molecular Genetics, Plant Biotechnology Center, and Center for RNA Biology, The Ohio State University, Columbus, Ohio, United States of America;State Key Laboratory of Rice Biology, Institute of Biotechnology, Zhejiang University, Hangzhou, People's Republic of China

关键词: DNA methylation;    Cytosine;    Genetically modified plants;    Leaves;    DNA-binding proteins;    Methylation;    Polymerase chain reaction;    Arabidopsis thaliana;   

DOI  :  10.1371/journal.ppat.1002329

学科分类：生物科学（综合）

来源: Public Library of Science

【 摘 要 】

DNA methylation is a fundamental epigenetic modification that regulates gene expression and represses endogenous transposons and invading DNA viruses. As a counter-defense, the geminiviruses encode proteins that inhibit methylation and transcriptional gene silencing (TGS). Some geminiviruses have acquired a betasatellite called DNA β. This study presents evidence that suppression of methylation-mediated TGS by the sole betasatellite-encoded protein, βC1, is crucial to the association of Tomato yellow leaf curl China virus (TYLCCNV) with its betasatellite (TYLCCNB). We show that TYLCCNB complements Beet curly top virus (BCTV) L2- mutants deficient for methylation inhibition and TGS suppression, and that cytosine methylation levels in BCTV and TYLCCNV genomes, as well as the host genome, are substantially reduced by TYLCCNB or βC1 expression. We also demonstrate that while TYLCCNB or βC1 expression can reverse TGS, TYLCCNV by itself is ineffective. Thus its AC2/AL2 protein, known to have suppression activity in other geminiviruses, is likely a natural mutant in this respect. A yeast two-hybrid screen of candidate proteins, followed by bimolecular fluorescence complementation analysis, revealed that βC1 interacts with S-adenosyl homocysteine hydrolase (SAHH), a methyl cycle enzyme required for TGS. We further demonstrate that βC1 protein inhibits SAHH activity in vitro. That βC1 and other geminivirus proteins target the methyl cycle suggests that limiting its product, S-adenosyl methionine, may be a common viral strategy for methylation interference. We propose that inhibition of methylation and TGS by βC1 stabilizes geminivirus/betasatellite complexes.

【 授权许可】

CC BY