Arabidopsis Histone Reader EMSY-LIKE 1 Binds H3K36 and Suppresses Geminivirus Infection

• DOI: 10.1128/jvi.00219-18
• Publication Date: 2018-06-04T09:46:03Z
• Authors: Tami Coursey; Milica Milutinovic; Elizabeth Regedanz; Jelena Brkljacic; David M. Bisaro
• Keywords: 0301 basic medicine; 570; EML1; Arabidopsis Proteins; Arabidopsis; 610; EML3; 3. Good health; Histones; 03 medical and health sciences; Geminiviridae; Host-Pathogen Interactions; Histone reader proteins; Geminivirus; Protein Binding

Histone posttranslational modifications (PTMs) impart information that regulates chromatin structure and activity. Their effects are mediated by histone reader proteins bind specific PTMs to modify and/or recruit appropriate effectors alter the landscape. Despite their crucial juxtaposition between functional outcome, relatively few plant readers have been identified, nothing is known about impact on viral pathogenesis. We used geminivirus Cabbage leaf curl virus (CaLCuV) as a model functionally characterize two recently identified proteins, EMSY-LIKE 1 (EML1) EML3, which contain Tudor-like Agenet domains predictive of PTM binding function. Here, we show mutant Arabidopsis plants exhibit contrasting hypersusceptible (eml1) tolerant (eml3) responses CaLCuV infection EML1 deficiency correlates with RNA polymerase II (Pol II) enrichment upregulated gene expression. Consistent activity, EML3 associate nucleosomes chromatin, suggesting direct also demonstrate peptides containing H3 lysine 36 (H3K36), usually associated active The interaction encompasses multiple H3K36 PTMs, including methylation acetylation, nuanced regulation. Furthermore, similar regions implying possible competition readers. Regions association correlate sites trimethylated (H3K36me3) enrichment, consistent regulation EML targeting.IMPORTANCE convey compaction DNA accessibility. translate modifying recruiting or In this study, was activities domain readers, EML3. eml1 mutants CaLCuV, whereas eml3 more than wild-type plants. histones in planta both H3K36, antiviral suppresses expression reduces Pol access chromatin. By linking pathogenesis, these studies expanded our knowledge uncovered an additional level