For a while there, it didn’t seem like long non-coding RNAS (lncRNAs) had very much to say on the subject of genomic imprinting. But some new evidence shows that lncRNAs have found their voice, shouting loud and clear as a cross-talk conduit between imprinted regions.
Researchers from Hebrew University (Jerusalem) introduced a new concept into the regulation of gene expression: the cross-talk of imprinted regions. The team reports in their latest paper the first clear cut example of this concept when they found that a paternally expressed lncRNA from one imprinted locus regulating the maternally expressed products from another.
In this intriguing case they have just shown how the SNRPN-UBE3A and DLK1-DIO3 imprinted clusters of ncRNA cross-talk via a novel lncRNA. Here’s what went down:
- First, induced pluripotent stem-cells (iPSCs) were derived from individuals with Prader-Willi Syndrome (PWS).
- Significant upregulation of maternally expressed genes was observed coming from the DLK1-DIO3 locus.
- This expression pattern was surprising since it stems from a seperate chromosome (14), shows an opposite imprinting pattern, and has not been implicated in PWS.
- Further study found a novel lncRNA from the PWS locus was regulating the transcripts from the other imprinted cluster.
- Altered transcripts coming from the DLK1-DIO3 locus correlate with chromatin modifications (H3K9me3) better than DNA methylation.
These findings suggest that some of the defining phenotypes attributed to the SNRPN-UBE3A locus may actually be consequences of the interruption of this regulatory cross-talk occurring between chromosomes via lncRNA.
Tune into the imprinted cross-talk over at Nature Genetics, May 2014