The Tnt1 Retrotransposon Escapes Silencing in Tobacco, Its Natural Host

• Published in: PloS one Vol. 7; no. 3; p. e33816
• Main Authors: Hernández-Pinzón, Inmaculada, Cifuentes, Marta, Hénaff, Elizabeth, Santiago, Néstor, Espinás, M. Lluïsa, Casacuberta, Josep M.
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 30.03.2012; Public Library of Science (PLoS)
• Subjects: Analysis; Arabidopsis; Biochemistry; Biology; Cell culture; Chromatin - metabolism; Deoxyribonucleic acid; DNA; DNA Methylation; Drosophila; Epigenesis, Genetic; Epigenetics; Gene expression; Gene Expression Regulation; Gene Order; Gene Silencing; Genes; Genetic aspects; Genetic engineering; Genetics; Genomes; Genomics; Histones - metabolism; Insects; Methylation; Methyltransferases - metabolism; Molecular biology; Mutagenesis; Nicotiana - genetics; Nicotiana - metabolism; Plant genetics; Plant viruses; Promoter Regions, Genetic; R&D; Research & development; Research parks; Retroelements - genetics; Stress, Physiological - genetics; Tobacco; Transcription (Genetics); Transcription, Genetic; Transgenes; Transposons; Viruses; Spain
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0033816

Retrotransposons' high capacity for mutagenesis is a threat that genomes need to control tightly. Transcriptional gene silencing is a general and highly effective control of retrotransposon expression. Yet, some retrotransposons manage to transpose and proliferate in plant genomes, suggesting that, as shown for plant viruses, retrotransposons can escape silencing. However no evidence of retrotransposon silencing escape has been reported. Here we analyze the silencing control of the tobacco Tnt1 retrotransposon and report that even though constructs driven by the Tnt1 promoter become silenced when stably integrated in tobacco, the endogenous Tnt1 elements remain active. Silencing of Tnt1-containing transgenes correlates with high DNA methylation and the inability to incorporate H2A.Z into their promoters, whereas the endogenous Tnt1 elements remain partially methylated at asymmetrical positions and incorporate H2A.Z upon induction. Our results show that the promoter of Tnt1 is a target of silencing in tobacco, but also that endogenous Tnt1 elements can escape this control and be expressed in their natural host.