In a paper published online in advance in Science this week, a large international research team describes how "transposon diversity, developmental gene repertoire, physical gene order, and intron-exon organization" indicate plasticity in the tunicate Oikopleura genome. The team also discusses the evolutionary consequences of genome compaction in Oikopleura. Further, the researchers suggest that the "ancestral architecture of animal genomes can be deeply modified and may therefore be largely non-adaptive." From sponges the humans, the team writes, "global similarities of genome architecture ... are not essential for the preservation of ancestral morphologies."
Matthew Scott and his colleagues at the University of California, San Diego, show that a theory incorporating the intrinsic constraints that govern the allocation of resources for protein synthesis in bacteria "can accurately predict how cell proliferation and gene expression affect one another, quantitatively accounting for the effect of translation-inhibiting antibiotics on gene expression and the effect of gratuitous protein expression on cell growth." Scott et al. suggest that using these empirical relations – which are "analogous to phenomenological laws" – could better researchers' understanding of complex biological systems in their pursuit of deciphering the regulatory circuits that underlie them.
An international team led by researchers at Japan's Riken Advanced Science Institute shows that Rickettsiella infection leads to a change in body color from red to green in pea aphids. Infection by the bacteria leads to an increase in the amount of blue-green polycyclic quinones while it affects yellow-red carotenoid pigments to a lesser extent. The Riken-led team infers that an ancient lateral gene transfer from Rickettsiella to the aphid genome is one of several factors that contribute to phenotypic variation within the insect's populations.
And in Science Translational Medicine this week, investigators in Italy and Canada report hematopoietic stem cell-specific microRNAs that enable gene therapy in globoid cell leukodystropy, a lysosomal storage disorder cause by GALC mutations. The team shows that miR-126, when incorporated into a GALC-expressing vector, can suppress the gene's expression in HSCs "while maintaining robust expression in mature hematopoietic cells." The authors write that the miR-126-mediated approach protects "HSCs from GALC toxicity" and, when applied to a mouse GLD model, it presents a "rational to explore HSC-based gene therapy" for the disease.