Changes to regulatory regions of the GDF6 gene may be behind the shape of the human foot, researchers from Stanford University School of Medicine and HudsonAlpha Institute for Biotechnology report in Cell. They traced differences in armor-plate size in stickleback fish to a cis-regulatory change in the GDF6 gene, finding that increased copies of GDF6 and higher expression levels lead to reduced armor size. Meanwhile, humans have lost a conserved regulatory element that usually controls GDF6 expression, the researchers report. In a mouse model, loss of this regulatory element leads to digit shortening, suggesting that this change could be why humans have small toes.
Transcriptional noise is mostly limited to the nucleus, according to a trio of University of Zurich researchers. The trio used a high-throughput automated single-molecule fluorescence in situ hybridization, or sm-FISH, approach they developed to examine variation in transcript abundance in single cells. From this, they note that variability in transcript abundance is minimally stochastic and that that variability is governed by multilevel transcript homeostasis in single cells. Further, they say that not only does nuclear compartmentalization allow for complex gene regulation as well as multicellularity, it also enables buffering of transcriptional noise and tighter gene expression control.
Finally, a University of Texas Southwestern Medical Center team reports in Cell that the long non-coding RNA NORAD sequesters PUMILIO proteins, which bind to and then repress the stability and translation of mRNAs, to regulate genomic stability. Inactivation of NORAD leads to aneuploidy, even in usually karyotypically stable cell lines. In its absence, PUMILIO represses mitotic, DNA repair, and DNA replication factors to generate chromosomal instability. This finding, the team says, adds to the idea that some lncRNAs act as molecular decoys.