A group of Princeton University and Caltech researchers write in Cell that small RNAs are involved in quorum-sensing pathways. The researchers found that the small RNA Qrr3 relies on four different mechanisms to influence its targets. For instance, it uses catalytic degradation to repress luxR, while using coupled degradation and sequestration to repress luxM and luxO, respectively. And it activates aphA by revealing the ribosome-binding site. "Combined mathematical modeling and experiments show that the specific Qrr regulatory mechanism employed governs the potency, dynamics, and competition of target mRNA regulation, which in turn, defines the overall quorum-sensing response," the researchers add.
Also in Cell, University of Cambridge researchers report that SOX17 is a key regulator of human primordial germ cell-like cells. The researchers derived such hPGCLS from germline-competent human embryonic stem cells and found that the expression profiles of the hPGCLCs they derived were consistent with actual human primordial germ cells. SOX17, they further report, regulates hPGC-like fate, while BLIMP1 represses endodermal and other genes during hPGCLCs derivation. This differs, the researchers note, from what occurs in mice, adding that this finding could affect the applicability of mouse cell fate studies to human cell fate.
The University of Toronto's Benjamin Blencowe and his colleagues examine alternative splicing in neurons, finding that microexons appear to be both highly conserved evolutionarily and employ a switch-like regulation. Most of these 3-nucleotide-to-15-nucleotide microexons modulate the function of interaction domains of proteins linked to neurogenesis and are regulated themselves by nSR100/SRRM4. In people with autism spectrum disorders, though, neural microexons are, though, misregulated. "The results thus reveal a highly conserved program of dynamic microexon regulation associated with the remodeling of protein-interaction networks during neurogenesis, the misregulation of which is linked to autism."