In PLOS Biology this week you can read about a survival strategy employed by Salmonella bugs, transcript capping in the cytoplasm and differences in the architecture of the visual cortex between rodents and higher mammals.
The mammalian visual cortex contains 50 to 100 thousand neurons per cubic millimetre, most of which are excitatory (85%) and the minority, inhibitory (15%). Unlike neurons in the retina, neurons in the visual cortex are preferentially activated by lines or edges of a particular orientation. In the visual cortex of higher mammals like cats and monkeys, neurons that share an orientation preference are clustered in functional columns. However, in rodents like mice, orientation preferences are randomly distributed. In a new study, Rita Bopp, Morgane Roth and colleagues asked whether the differences between columnar and non-columnar cortex are correlated with differences in the connectivity patterns between excitatory and inhibitory neurons in mice. Their results show that the ratio of excitatory-inhibitory neurons in the mouse visual cortex is similar to that of cat or monkey visual cortex, but in the mouse local pyramidal neurons target proportionately many more inhibitory neurons compared to other studies in higher mammals. This suggests that inhibition may stand in for columns as the organising principle.
Bacterial populations grow rapidly and asexually, generating millions of genetically identical progeny. However despite genetic and environmental uniformity, we now know that differences can occur, through stochastic molecular processes. But what are the advantages of this in a group of clonal organisms? Markus Arnoldini, Martin Ackermann and colleagues studied the human pathogen Salmonella typhimurium, which is known to vary in levels of virulence factors called ttss-1. Those bugs which express high levels of the factor grow slower, but the authors showed that they were also better able to survive antibiotic treatments. So it seems that this is a ‘bet-hedging’ strategy that pays off when disaster strikes. This has implications for antibiotic use, as selection for tolerance of the drug might also inadvertently select for high virulence. Read more in the accompanying synopsis.
Messenger RNA ‘capping’ was previously thought to happen only in the nucleus, with subsequent degradation in the cytoplasm. However there has been recent evidence of capping taking place in the cytoplasm. In this week’s issue of PLOS Biology work by Chandrama Mukherjee, Baskar Bakthavachalu and Daniel Schoenberg build on this discovery. They have identified a domain of the cytoplasmic Capping Enzyme, which is required for its function in cytoplasmic capping. This allows it to bind to the adapter protein Nck1 – Nck1 is better known as a player in kinase-mediated signalling pathways, but here they show that it also helps provide a scaffold for assembly of the cytoplasmic capping complex.