Researchers from the University of Illinois at Chicago have identified a molecular switch that converts skin cells into cells that make up blood vessels, which could ultimately be used to repair damaged vessels in patients with heart disease or to engineer new vasculature in the lab. The technique, which boosts levels of an enzyme that keeps cells young, may also circumvent the usual aging that cells undergo during the culturing process. Their findings are reported in the journal Circulation. Rest – April 6, 2017
SAN FRANCISCO, April 17, 2017 /PRNewswire/ — Twist Bioscience, a company accelerating science and innovation through rapid, high-quality DNA synthesis, today announced Microsoft Corp. will purchase ten million strands of DNA from Twist Bioscience for expanded digital data storage research. The strands of DNA will be long-chain oligonucleotides used by researchers at Microsoft and the University of Washington to encode digital data at higher density. After working together for over a year, the organizations have improved storage density, thereby reducing the cost of DNA digital data storage by encoding more data per strand and increasing the throughput of DNA production. Rest
Prestigious Japan Prize goes to Max Planck scientist for a third time
February 06, 2017 – It is often referred to as the Japanese Nobel Prize: 88 prize winners from 13 countries have received it since it was awarded for the first time in 1985 – including many later Nobel Prize Laureates. Emmanuelle Charpentier from the Max Planck Institute for Infection Biology, Berlin, and Jennifer A. Doudna from the University of California, Berkeley, receive this year’s Japan Prize for the development of the CRISPR-Cas9 gene-editing technique, a type of very efficient genetic ‘scissors’. Adi Shamir, from the Weizmann Institute, Israel, is honoured for his pioneering research on cryptography. The award ceremony will take place on April 19 at the National Theater in Tokyo. Rest
3-4 April 2017, London.Gala Dinner 3 April, The Crypt, St Paul’s.
The field of Nanomedicine continues to accelerate, and several trans-European research endeavours are focused on delivering benefits to patients. Nanomedicine promises to bring about a paradigm shift in the treatment and diagnosis of disease, with emerging technologies being explored across a number of diseases and indications. After a very successful edition of the European Nanomedicine Meeting in Grenoble in 2015, the British Society for Nanomedicine is proud to work with European colleagues to host ENM2017 in London.The European Nanomedicine Meeting 2017 will take place on the 3rd and 4th of April 2017 at Kings College London, UK.
The meeting will provide a forum for international exchange of research to facilitate translation and innovation in nanomedicine research and development. Leading experts and international stakeholders will have the opportunity to discuss opportunities and challenges in this exciting new field of medicine. The meeting will provide delegates with a pulse on the latest developments, as well as a systematic understanding of new nanomedicine paradigms across the development pathway.
Don’t miss this opportunity to participate in the second edition of the European Nanomedicine Meeting in London! MORE
In 5 years, new medical labs on a chip will serve as nanotechnology health detectives – tracing invisible clues in our bodily fluids and letting us know immediately if we have reason to see a doctor. The goal is to shrink down to a single silicon chip all of the processes necessary to analyze a disease that would normally be carried out in a full-scale biochemistry lab. Rest
Abstract: Binding of the Origin Recognition Complex (ORC) to origins of replication marks the first step in the initiation of replication of the genome in all eukaryotic cells. Here, we report the structure of the active form of human ORC determined by X-ray crystallography and cryo-electron microscopy. The complex is composed of an ORC1/4/5 motor module lobe in an organization reminiscent of the DNA polymerase clamp loader complexes. A second lobe contains the ORC2/3 subunits. The complex is organized as a double-layered shallow corkscrew, with the AAA+ and AAA+-like domains forming one layer, and the winged-helix domains (WHDs) forming a top layer. CDC6 fits easily between ORC1 and ORC2, completing the ring and the DNA-binding channel, forming an additional ATP hydrolysis site. Analysis of the ATPase activity of the complex provides a basis for understanding ORC activity as well as molecular defects observed in Meier-Gorlin Syndrome mutations. Full article
A global research team has built five new synthetic yeast chromosomes, meaning that 30 percent of a key organism’s genetic material has now been swapped out for engineered replacements. This is one of several findings of a package of seven papers published March 10 as the cover story for Science.
Led by NYU Langone geneticist Jef Boeke, PhD, and a team of more than 200 authors, the publications are the latest from the Synthetic Yeast Project (Sc2.0). By the end of this year, this international consortium hopes to have designed and built synthetic versions of all 16 chromosomes—the structures that contain DNA—for the one-celled microorganism Baker’s yeast, known as S. cerevisiae.
Like computer programmers, scientists add swaths of synthetic DNA to—or remove stretches from—human, plant, bacterial, or yeast chromosomes in hopes of averting disease, manufacturing medicines, or making food more nutritious. Baker’s yeast have long served as an important research model because their cells share many features with human cells, but are simpler and easier to study. Rest
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