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Category: genetics – Page 480

Researchers have discovered a way to program cells to inhibit CRISPR-Cas9 activity. “Anti-CRISPR” proteins had previously been isolated from viruses that infect bacteria, but now University of Toronto and University of Massachusetts Medical School scientists report three families of proteins that turn off CRISPR systems specifically used for gene editing. The work, which appears December 15 in Cell, offers a new strategy to prevent CRISPR-Cas9 technology from making unwanted changes.

“Making CRISPR controllable allows you to have more layers of control on the system and to turn it on or off under certain conditions, such as where it works within a cell or at what point in time,” says lead author Alan Davidson, a phage biologist and bacteriologist at the University of Toronto. “The three anti-CRISPR proteins we’ve isolated seem to bind to different parts of the Cas9, and there are surely more out there.”

CRISPR inhibitors are a natural byproduct of the evolutionary arms race between viruses and bacteria. Bacteria use CRISPR-Cas complexes to target and cut up genetic material from invading viruses. In response, viruses have developed proteins that, upon infection, can quickly bind to a host bacterium’s CRISPR-Cas systems, thus nullifying their effects.

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The following press release was written and and published by the Defense Advanced Research Projects Agency (DARPA) and originally published on their website. Click here to see the original version of this post.

On a recent sunny fall day in the nation’s capital, several hundred volunteers—each toting a backpack containing smartphone-sized radiation detectors—walked for hours around the National Mall searching for clues in a “whodunit” scavenger hunt to locate a geneticist who’d been mysteriously abducted. The geneticist and his abduction were fictitious. But the challenge this scavenger hunt was designed to address is real: The need to detect even small quantities of radioactive material that terrorists might try to bring into an urban area with the intent of detonating a “dirty bomb,” or worse. By getting volunteers to walk all day looking for clues, the DARPA-sponsored exercise provided the largest test yet of DARPA’s SIGMA program, which is developing networked sensors that can provide dynamic, real-time radiation detection over large urban areas.

A key element of SIGMA, which began in 2014, has been to develop and test low-cost, high-efficiency, radiation sensors that detect gamma and neutron radiation. The detectors, which do not themselves emit radiation, are networked via smartphones to provide city, state, and federal officials real-time awareness of potential nuclear and radiological threats such as dirty bombs, which combine conventional explosives and radioactive material to increase their disruptive potential. Following a demonstration earlier this year with the Port Authority of New York and New Jersey involving more than 100 SIGMA sensors, the 1,000-detector deployment in Washington, D.C., marked the largest number of SIGMA mobile detectors ever tested at one time and was a demonstration of the program’s ability to fuse the data provided by all those sensors to create minute-to-minute situational awareness of nuclear threats.

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Why Synbio computing is where we ultimately want to more and more progress towards especially once the basic infrastructure is updated with technology like QC.

Cells are often likened to computers, running an operating system that receives signals, processes their input, and responds, according to programming, with cellular output. Yet untangling computer-like pathways in cells is anything but simple, say Denise Montell, professor at the University of California, Santa Barbara, and Aviv Regev, a Howard Hughes Medical Institute investigator at the Massachusetts Institute of Technology and the Broad Institute. However, both are eager to try and will outline their latest efforts at the “Logic of Signaling” symposium at the 2016 ASCB Annual Meeting.

“My lab is understanding how cells maintain and build normal tissues. We’re studying cellular behaviors that underlie normal behavior and tumor metastasis, a great unsolved question in cancer,” Montell said. Her lab recently discovered that cells can bounce back from the brink of apoptotic cell death. “This wasn’t known before so now we’re looking at how cells do it, when do they do it, under what circumstances, and what does it mean,” Montell said.

To track these near-death experiences in cells the Montell lab generated a genetically coded sensor in Drosophila. The researchers expected the mechanism to be a stress response, but they found that it was normal during development. “It makes sense retrospectively,” Montell explained, pointing to neuronal development as an example. “You produce way more neurons that you need, and the neurons compete for trophic factors. If a group of cells are competing for trophic factors, then one cell starts to die, but if it gets more trophic factor, it could bounce back.”

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In Brief

  • By observing the transparent cells of roundworms, researchers have uncovered a link between lifespan and the natural cellular process of RNA splicing.
  • This research could lead to new breakthroughs in anti-aging treatments that would allow humans to indefinitely keep ourselves healthy, stalling death for as long as possible.

Though aging seems like one of the most natural things, an affair common to all living creatures, the process is actually poorly understood by scientists. A new study detailed in Nature aims to shed light on the phenomenon as a research team led by the Harvard T.H. Chan School of Public Health has uncovered a relationship between lifespan and RNA splicing, a core function of cells that allows a single gene to produce a variety of proteins.

The researchers already knew that mutations in RNA splicing could lead to disease, but they wanted to find out if the act of splicing itself had an impact on the aging process. To find out, they designed experimental setups using the roundworm Caenorhabditis elegans, which show visible signs of aging during their short three-week lifespan.

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Great.

Research published in Acta Neuropathologica, identified alterations in a protein known as ATRX in human brain tumours; researchers might also be able to target microRNAs directly, altering their levels to make cancer cells less likely to form tumours.

A recent study suggests that two recently discovered genetic differences between brain cancer cells and normal tissue cells could offer clues to tumour behaviour and potential new targets for therapy.

Published in Acta Neuropathologica, the study identified alterations in a protein known as ATRX in human brain tumours that arise as part of a genetically inherited condition known as neurofibromatosis type 1 (NF1). The disorder, marked initially by benign tumours on nerves, often leads to brain cancer, and although most NF1-related malignancies are nonaggressive, a fraction are “high-grade” and difficult to treat, experts say.

Continue reading “Research sets new target for brain cancer therapy” | >