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Title: Trans-Reactivation: A New Epigenetic Phenomenon Underlying Transcriptional Reactivation of Silenced Genes}
Article:
Abstract:
In order to study the role played by cellular RNA pools produced by homologous genomic loci in defining the transcriptional state of a silenced gene, we tested the effect of non-functional alleles of the white gene in the presence of a functional copy of white, silenced by heterochromatin. We found that non-functional alleles of white, unable to produce a coding transcript, could reactivate in trans the expression of a wild type copy of the same gene silenced by heterochromatin. This new epigenetic phenomenon of transcriptional trans-reactivation is heritable, relies on the presence of homologous RNA’s and is affected by mutations in genes involved in post-transcriptional gene silencing. Our data suggest a general new unexpected level of gene expression control mediated by homologous RNA molecules in the context of heterochromatic genes.
Introduction:
In recent years it has become increasingly evident that the expression of eukaryotic genomes is far more complex than it had been previously explored. An emerging body of evidence, coming from next generation sequencing approaches, is showing that the genomes of all studied eukaryotes are almost entirely transcribed, generating an enormous number of non-coding RNAs( ncRNAs)[1]. The ENCODE project showed that at least 90% of analyzed eukaryote genome is transcribed in different cell types, indicating that there is a huge reservoir of RNA molecules with potentially unexplored biological function[2, 3, 4]. These RNAs are remarkably different in their number, size, subcellular localization, and mechanisms of action, and many are essential to finely control gene expression as well as genomic plasticity[5]. It is becoming increasingly clear that some ncRNAs are part of epigenetic regulatory networks with striking evolutionary conservation[6, 7]. For example, dynamic changes in chromatin function are frequently transacted by nuclear RNA signaling pathways. Although the evolutionarily conservation and precise molecular mechanisms are poorly understood, a differential recruitment of a hierarchy of chromatin modifying complexes to specific loci by RNAs sets precise transcriptional states leading to differentiation[8, 9, 10, 11, 12]. Moreover, the unusual epigenetic phenomena of paramutation[13, 14, 15], trans-induction[16] and transvection[17, 18] observed in a variety of higher eukaryotes involve the activity of ncRNAs that ‘rewrite’ the transcriptional state of an allele, in processes that apparently escape classic Mendel’s laws of genetic inheritance. These epigenetic phenomena are clear examples of ncRNA-directed regulatory processes that transfer epigenetic information both across cells, between tissues and across generations, though the mechanisms underlying these phenomena still remain elusive. In order to unveil the role played by cellular RNA pools produced by homologous genomic loci in changing the transcriptional state of a silenced gene, we used classic Position Effect Variegation( PEV) assays in the model system D. melanogaster[19, 20] and tested the effect of non-functional alleles of the white gene in the presence of a functional copy of white, silenced by heterochromatin( wm4h). Surprisingly, we found that several non-functional white alleles, unable to produce the main wildtype white coding transcript but with the potential of transcribing other RNA’s from the white locus, trans-reactivate the variegating wm4h line thus increasing eye pigmentation. Strikingly, the presence of non-functional white alleles cause an increase in the wm4h gene transcript as well as an opening in the chromatin structure at the wm4h locus. Remarkably, this new epigenetic phenomenon is heritable, relies on the presence of diffusible homologous RNA’s, and is affected by mutations in genes involved in post-transcriptional gene silencing. Overall, our data strongly indicate that trans-reactivation is a new epigenetic phenomenon that positively control gene expression in the context of heterochromatin through homologous RNA molecules.
Discussion:
Over the last decade we have come to appreciate that the eukaryotic chromatin is full of coding and non-coding overlapping transcripts, and that a lot of the genetic information is transacted by coding and non-coding RNAs. Indeed, the vast majority of genomes of all metazoans are transcribed into complex patterns of ncRNAs. Recent observations strongly suggest that ncRNAs contribute to the complex transcriptional networks needed to regulate cell function[36, 37]. However, despite a rich variety of mechanisms by which RNA acts by repressing transcription have been identified, fewer studies have explored the role of RNA in the positively regulation of transcription. RNA is an integral component of chromatin[38] and many transcription factors and chromatin modifying enzymes have the capacity to bind RNA or complexes containing RNA or RNA-binding proteins[8]. Moreover, RNA-directed processes help to establish chromatin architecture and epigenetic memory[10]. Indeed, ncRNAs can act locally to regulate the epigenetic state of the nearby chromatin, often recruiting either repressing or activating chromatin remodeling complexes[8]. Given the high degree of sequence and locus specificity information, RNA could recruit chromatin remodelers and modifiers in a sequence-specific manner. Indeed, recent observations are beginning to reveal that RNA molecules can stimulate gene transcription. These RNA activators employ a wide array of mechanisms to up-regulate transcription of target genes, often functioning as DNA-tethered activation domains, as coactivators or modulators of general transcriptional machinery[39]. In search for a possible role played by cellular RNA pools produced by homologous genomic loci in changing the transcriptional state of a silenced gene, we found that non-functional alleles of the classic fly marker white could trans-reactivate the expression of wild type copy of white silenced by heterochromatin. We called this new epigenetic phenomenon trans-reactivation. This process is heritable over many generations, it relies on the presence of diffusible RNAs, and it is affected by mutations in genes involved in post-transcriptional gene silencing. Our data strongly suggest that the presence of a gene that does not produce a full coding transcript but only spurious transcription could trans-reactivate the expression of a functional copy of the same gene silenced by heterochromatin, defining a new unpredicted level of gene expression control in the context of heterochromatic genes. The mechanisms of action and many features of trans-reactivation appear to be different from the previously characterized epigenetic reprogramming events occurring in paramutation, transinduction and transvection. In trans-reactivation genomic regions, transcribing RNAs unable to produce a full coding transcript, can positively influence the transcriptional state of an homologous locus silenced by heterochromatin. However, how can the information present in the non-functional RNA molecules be ‘read’ and telecasted to specific silenced homologous genomic regions? RNA molecules have the potential to pair with other RNA molecule or with DNA. Possibly through their ability to form paired structures, RNA may function as a sensor and/or a messenger of homology. RNA can form duplexes with sequence homology with genomic promoter sequences thus promoting transcription[40]. Indeed, there is a great deal of evidence that enhancers and other promoter regulatory sequences are transcribed in the cell in which they are active, and that enhancer transcription is often needed to activate the transcription on their target gene[41]. Moreover, given that mutations in genes encoding for factors involved in posttranscriptional gene silencing modulate trans-reactivation, it remains to be determined whether some sequence specific small ncRNAs, that we failed to identify, may explain the mechanism of trans-reactivation. Furthermore, we do not know why some non-functional w* null or hypomorphic alleles failed to trans-reactivate their homologous silenced locus. Indeed, differences in trans-reactivation ability between different w* alleles will need future investigation, and may provide key information to understand the mechanism of action of trans-reactivation. However, independently from the mechanistic details of trans-reactivation, we are convinced that we identified a new epigenetic phenomenon of allelic communication that acts through diffusible RNA molecules. Nevertheless, much work need to be done to study the evolutionary conservation and the general ability of trans-reactivating RNAs in resetting the epigenetic and transcriptional state of homologous genetic loci.
We discovered a new epigenetic phenomenon we called trans-reactivation . We found that genes , unable to produce a functional coding transcript , but with the potential of transcribing other RNA’s within their gene body , strongly reactivate the transcription of a wildtype copy of the same gene silenced by heterochomatin . This new epigenetic phenomenon is heritable , relies on the presence of diffusible RNAs able to carry and transfer epigenetic information and is affected by mutations in genes involved in Post-Transcriptional Gene Silencing . Our data strongly suggest that homologous non-coding RNA can reactivate the expression of genes silenced by heterochromatin , thus defining a new unpredicted level of gene expression control in the context of heterochromatic genes .