In Science this week, researchers in the US and Chile report a method of producing biofuel from brown macroalgae using microbes. The team discovered a 36-kilobase pair DNA fragment in Vibrio splendidus that encodes enzymes for alginate transport and metabolism. "The genomic integration of this ensemble, together with an engineered system for extracellular alginate depolymerization, generated a microbial platform that can simultaneously degrade, uptake, and metabolize alginate," the authors write. "When further engineered for ethanol synthesis, this platform enables bioethanol production directly from macroalgae via a consolidated process, achieving a titer of 4.7 percent volume/volume and a yield of 0.281 weight ethanol/weight dry macroalgae."
Also in Science this week, researchers in France report observing polymerase exchange in living E. coli cells, during Okazaki fragment synthesis. The team observed "repetitive fluorescence bursts of single polymerase IIIs," which suggested a polymerase exchange was taking place at the replication fork. "Fluctuations in the amount of DNA-bound single-stranded DNA-binding protein reflect different speeds for the leading- and lagging-strand DNA polymerases," the authors write. "Coincidence analyses of Pol III and SSB fluctuations show that they correspond to the lagging-strand synthesis and suggest the use of a new Pol III for each Okazaki fragment." These results could lead to the conclusion that the third polymerase in the replisome plays a role in lagging-strand synthesis, they add.
In Science Signaling this week, researchers in Japan and Australia report the association of oxidative stress and compensatory proliferation through interleukin-11. In the study, the team shows that IL-11 is produced by cells in an oxidative stress-dependent manner, and that its production depends on the activation of extracellular signal–regulated kinase 2 in dying cells. This kinase, in turn, causes phosphorylation and accumulation of transcription factor Fra-1, the authors write, which is then recruited to the IL-11 promoter. "Upon acute liver injury in mice, IL-11 was mainly produced by hepatocytes in response to reactive oxygen species that were presumably released from dying hepatocytes," the team writes. "IL-11 that was secreted by the dying cells then induced the phosphorylation of the transcription factor STAT3 in adjacent healthy hepatocytes, which resulted in their compensatory proliferation. Furthermore, an IL-11 receptor agonist enhanced the proliferation of hepatocytes and ameliorated oxidative stress upon acetaminophen-induced liver injury."
Finally, in Science Translational Medicine this week, researchers at the University of California, San Francisco, and Cornell University say the normalization of Notch4 can reduce the size of blood vessels in arteriovenous malformations. The team studied mouse brain arteriovenous shunts caused by the up-regulation of Notch signaling in endothelial cells, and found that "normalizing Notch signaling by repressing Notch4 expression converted large-caliber, high-flow AV shunts to capillary-like vessels." In addition, structural regression of the AV shunts reversed the tissue hypoxia by returning blood to the capillaries. "Normalization of Notch signaling resulting in regression of high-flow AV shunts, and a return to normal blood flow suggests that targeting the Notch pathway may be useful therapeutically for treating diseases such as AVMs," the authors write.