Abstract
Mutations in REPRESSOR OF SILENCING1 (ROS1) lead to the transcriptional gene silencing (TGS) of Pro(RD29A):LUC (LUCIFERASE) and Pro(35S):NPTII (Neomycin Phosphotransferase II) reporter genes. We performed a genetic screen to find suppressors of ros1 that identified two mutant alleles in the Arabidopsis (Arabidopsis thaliana) CHLOROPHYLL A/B BINDING PROTEIN UNDEREXPRESSED1 (CUE1) gene, which encodes a plastid inner envelope phosphoenolpyruvate/phosphate translocator. The cue1 mutations released the TGS of Pro(35S):NPTII and the transcriptionally silent endogenous locus TRANSCRIPTIONAL SILENCING INFORMATION in a manner that was independent of DNA methylation but dependent on chromatin modification. The cue1 mutations did not affect the TGS of Pro(RD29A):LUC in ros1, which was dependent on RNA-directed DNA methylation. It is possible that signals from chloroplasts help to regulate the epigenetic status of a subset of genomic loci in the nucleus.
Highlights
Mutations in REPRESSOR OF SILENCING1 (ROS1) lead to the transcriptional gene silencing (TGS) of ProRD29A:LUC (LUCIFERASE) and Pro35S:NPTII (Neomycin Phosphotransferase II) reporter genes
Heterochromatin can lead to transcriptional gene silencing (TGS), which plays a central role in repressing transposon movement and mediating gene repression during developmental and cellular differentiation in plants (Martienssen and Colot, 2001; Henderson and Jacobsen, 2007; Matzke et al, 2007, 2009)
In the DNA methylationindependent pathway, several proteins involved in DNA replication and repair regulate the epigenetic status of the transcriptionally silent endogenous locus TRANSCRIPTIONAL SILENCING INFORMATION (TSI) in Arabidopsis (Arabidopsis thaliana)
Summary
Previous studies suggest that several retrograde signaling pathways transducing signals from chloroplasts to the nucleus regulate the expression of genes that function within the chloroplast (Nott et al, 2006; Koussevitzky et al, 2007; Pesaresi et al, 2007). Blocking small RNA production in ros releases the TGS of ProRD29A:LUC but not that of Pro35S:NPTII, suggesting that these two loci possess different TGS mechanisms (Kapoor et al, 2005; Xia et al, 2006; Wang et al, 2007; He et al, 2009). Mutations in CUE1 influenced the histone H3K9 dimethylation and H3 acetylation only at some loci, suggesting that these signals produced by CUE1 mutations influence TGS independent on DNA methylation, probably by modulating histone modifications in the affected loci, but did not affect global histone modifications Proteins such as BRU1, FAS1, FAS2, RPA2A/ROR1, ABO4/DNA polymerase «, TSL, and MORPHEUS# MOLECULE1 (MOM1) are required for maintenance of TGS at TSI independent of DNA methylation (Takeda et al, 2004; Elmayan et al, 2005; Kapoor et al, 2005; Shaked et al, 2006; Xia et al, 2006; Wang et al, 2007). Such coordination may be required for appropriate short-term responses to environmental changes and possibly for long-term, evolutionary adaptation to environmental stresses by eliciting epigenetic changes (Yin et al, 2009)
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