Poster abstracts
Poster number 48 submitted by Elizabeth Regedanz
Regulation of a geminivirus late gene promoter by PRC2
Elizabeth Regedanz (Department of Molecular Genetics, Center for Applied Plant Sciences, Center for RNA Biology, and Infectious Diseases Institute, The Ohio State University, Columbus, OH 43210), Mary Berger (Department of Biology and South Texas Center for Emerging Infectious Diseases, University of Texas-San Antonio, San Antonio, TX 78249), Garry Sunter (Department of Biology and South Texas Center for Emerging Infectious Diseases, University of Texas-San Antonio, San Antonio, TX 78249), David M. Bisaro (Department of Molecular Genetics, Center for Applied Plant Sciences, Center for RNA Biology, and Infectious Diseases Institute, The Ohio State University, Columbus, OH 43210)
Abstract:
Geminiviruses are small ssDNA viruses that cause significant yield loss in many agriculturally important crops. Upon entry into the nucleus, the viral genome is converted by host enzymes into a dsDNA replicative form (RF). The RF associates with histones to form non-integrating episomes that both facilitate virus replication and transcription and serve as targets of host defense pathways. As viral chromatin is formed de novo in infected cells, geminiviruses are unique models for examining mechanisms that target and establish epigenetic modifications. Polycomb Repressive Complex 2 (PRC2) is an important repressive regulator of developmental processes via its ability to deposit histone H3 lysine 27 trimethylation (H3K27me3), but how PRC2 activity is regulated at target genes is unclear. We propose that geminivirus gene expression is a model for PRC2 control, as we have found that H3K27me3 is localized to the viral coat protein (CP) promoter, which is repressed early in infection. We have also found that the CP promoter is bound by the plant-specific transcription factor TCP24, which has been implicated in PRC2 recruitment. Importantly, TCP24 mRNA levels decrease in geminivirus-infected cells. Thus, we hypothesize that TCP24 recruits PRC2 to inhibit premature CP expression and permit viral genome amplification. Once a threshold of genomes is produced, reduced TCP24 levels allow CP expression, leading to virion assembly. Thus, our studies offer insight into the temporal control of the geminivirus infection cycle, as well as principles underlying developmental gene regulation.
Keywords: Geminivirus Coat Protein Expression, PRC2, H3K27me3