Scientists at The Scripps Research Institute (TSRI) have announced the development of the first stable semisynthetic organism. Building on their 2014 study in which they synthesized a DNA base pair, the researchers created a new bacterium that uses the four natural bases (called A, T, C and G), which every living organism possesses, but that also holds as a pair two synthetic bases called X and Y in its genetic code.
TSRI Professor Floyd Romesberg and his colleagues have now shown that their single-celled organism can hold on indefinitely to the synthetic base pair as it divides. Their research was published January 23, 2017, online ahead of print in the journal Proceedings of the National Academy of Sciences. Rest
Now, for the first time, scientists from Harvard Medical School have managed to “listen in” on the crosstalk between individual microbes and the entire cast of immune cells and genes expressed in the gut.
The experiments, published Feb. 16 in Cell, provide a blueprint for identifying important microbial influencers of disease and health and can help scientists develop precision-targeted treatments.
Past research has looked at links between disease and the presence or absence of certain classes of bacteria in the gut. By contrast, the HMS team homed in on one microbe at a time and its effects on nearly all immune cells and intestinal genes, an approach that offers a more precise understanding of the interplay between individual gut microbes and their hosts. Beyond that, the team said, the approach could help scientists screen for molecules or bacterial strains that can be used therapeutically to fine-tune certain immune responses.
“We set out to map out interactions between bacteria and the immune system in the hope that this could eventually lead to the development of an apothecary of agents tailored to modulate the immune system selectively and precisely,” said senior investigator Dennis Kasper, professor of medicine and microbiology and immunobiology at HMS. Rest
Abstract: Natural Killer (NK) cells are essential for control of viral infection and cancer. NK cells express NKG2D, an activating receptor that directly recognizes NKG2D ligands. These are expressed at low level on healthy cells, but are induced by stresses like infection and transformation. The physiological events that drive NKG2D ligand expression during infection are still poorly understood. We observed that the mouse cytomegalovirus encoded protein m18 is necessary and sufficient to drive expression of the RAE-1 family of NKG2D ligands. We demonstrate that RAE-1 is transcriptionally repressed by histone deacetylase inhibitor 3 (HDAC3) in healthy cells, and m18 relieves this repression by directly interacting with Casein Kinase II and preventing it from activating HDAC3. Accordingly, we found that HDAC inhibiting proteins from human herpesviruses induce human NKG2D ligand ULBP-1. Thus our findings indicate that virally mediated HDAC inhibition can act as a signal for the host to activate NK-cell recognition. DOI: 10.7554/eLife.14749.001