Transcription requires chromatin to be in the unwound, open-access state. Boundary elements create a roadblock to remodeling machinery to prevent euchromatin from improperly converting back to tightly wound heterochromatin, and vice versa. Now, Victoria Lunyak, Geoff Rosenfeld (University of California, San Diego, CA), and colleagues reveal that boundary elements can be created by the transcription of noncoding repeat sequences derived from retrotransposons.
Lunyak et al. were dissecting the unwinding and regulation of the mouse growth hormone gene (GH). They mapped histone modifications that mark the transition to unwound chromatin to a region far upstream of the gene's enhancer—a spot containing a short interspersed nuclear element (SINE) B2 repeat. SINE B2 repeats are best known as retrotransposon-derived pseudogenes of the tRNA gene that are uniquely transcribed on opposite strands by RNA polymerases II and III.
Enhancer-blocking assays confirmed the sequence's role as a boundary element. Deleting the short sequence, which is about the length of one nucleosome, left GH in a permanently heterochromatic state.
Most known vertebrate boundary elements recruit proteins that form the chromatin roadblock. It is unknown what triggers the bidirectional transcription of SINE B2, but boundary activity only occurred when both transcription machineries were in play. The authors also found that the boundaries were created by the double transcription, not the transcripts. Lunyak suggests that this boundary strategy might be sprinkled throughout the mouse and human genomes where SINE-type repeats exist.