In PLoS Biology this week, investigators at the University of Toronto report that most "dark matter" transcripts are associated with known genes in the mouse and human genomes. Using a combination of RNA-seq information and data obtained from tiling arrays experiments, the team shows that most of the seqfrags — or transcribed regions outside known exons and non-coding RNAs — are within introns, "raising the possibility that they are fragments of pre-mRNAs," they write. While new intergenic transcripts do exist, "their number and abundance is generally low in comparison to known exons, and the genome is not as pervasively transcribed as previously reported," the authors suggest.
Meanwhile, in PLoS Genetics, researchers in the US and Israel report they survey of genomic traces, which revealed a common sequencing error — G to A — as well as RNA and DNA editing in sequences from the National Center for Biotechnology Information's Trace Archive and other databases. The team also uncovered "thousands of mismatch clusters with no apparent defects in their chromatograms," which elucidated "RNA editing in human and mouse and also revealing, for the first time, extensive RNA editing in Xenopus tropicalis," the team writes.
Research published in PLoS One this week shows that "microRNA expression patterns reveal differential expression of target genes with age." In profiling the expression of more than 800 miRNAs in peripheral blood mononucelear cells using real-time PCR, investigators at the National Institute on Aging show that "the majority of miRNAs studied decreased in abundance with age." They also identified nine miRNAs that were expressed at much lower levels in older individuals — five of which have previously been implicated in cancer pathogenesis, therefore suggesting that "miRNAs and their predicted targets have the potential to be diagnostic indicators of age or age-related diseases," they conclude.
Also in PLoS One this week, researchers report their elucidation of a SALL4/OCT4 transcriptional feedback network which affects the pluripotency — or "stemness," as they write — of embryonic stem cells. "SALL4 is a master regulator that controls its own expression and the expression of OCT4," the authors write, adding their discovery that "SALL4 and OCT4 work antagonistically to balance the expressions of other SALL gene family members."