The latest DNA nanodevices created at the Technische Universitaet Muenchen (TUM)—including a robot with movable arms, a book that opens and closes, a switchable gear, and an actuator—may be intriguing in their own right, but that's not the point. They demonstrate a breakthrough in the science of ...
Cell death and differentiation is a monthly research journal focused on the exciting field of programmed cell death and apoptosis. It provides a single accessible source of information for both scientists and clinicians, keeping them up-to-date with advances in the field. It encompasses programmed cell death, cell death induced by toxic agents, differentiation and the interrelation of these with cell proliferation.
Human colorectal tumors bear recurrent mutations in genes encoding proteins operative in the WNT, MAPK, TGF-β, TP53 and PI3K pathways1, 2. Although these pathways influence intestinal stem cell niche signaling3, 4, 5, the extent to which mutations in these pathways contribute to human colorectal carcinogenesis remains unclear. Here we use the CRISPR-Cas9 genome-editing system6, 7 to introduce multiple such mutations into organoids derived from normal human intestinal epithelium. By modulating the culture conditions to mimic that of the intestinal niche, we selected isogenic organoids harboring mutations in the tumor suppressor genes APC, SMAD4 andTP53, and in the oncogenes KRAS and/or PIK3CA. Organoids engineered to express all five mutations grew independently of niche factors in vitro, and they formed tumors after implantation under the kidney subcapsule in mice. Although they formed micrometastases containing dormant tumor-initiating cells after injection into the spleen of mice, they failed to colonize in the liver. In contrast, engineered organoids derived from chromosome-instable human adenomas formed macrometastatic colonies. These results suggest that 'driver' pathway mutations enable stem cell maintenance in the hostile tumor microenvironment, but that additional molecular lesions are required for invasive behavior.
Scientists have discovered a way to enhance the efficiency of CRISPR genome editing with the introduction of a few key chemical compounds. This has important potential implications for correcting disease-causing genetic mutations.
With a few easy tweaks, scientists can cut-and-paste DNA inside living cells, thanks to a promising new technique that could make possible everything from testing new drugs or curing genetic diseases. And researchers just discovered a way to make...
Alasdair Russell's insight:
Cheap genome-wide libraries for all - CRISPR EATER
Precise genome engineering in live cells at any locus promises to facilitate basic research and to enable personalized medicine. In particular, the recent development of the CRISPR-Cas9 system into a versatile and easy-to-use editing tool1 has been celebrated as a scientific breakthrough in the field. As genome engineering is adapted to clinical applications, a high level of precision—especially the avoidance of editing at sites other than the intended target—will be indispensable. In this issue, three very timely studies2, 3, 4 report methods for identifying off-target double-strand breaks produced by CRISPR-associated (Cas)9 nucleases and another class of programmable nucleases known as transcription activator–like effector nucleases (TALENs). Wang et al.2 and Tsai et al.3 rely on integration of a foreign DNA bait sequence into off-target double-strand breaks, whereas Frock et al.4 detect translocations of endogenous genomic sequences to the intended cleavage site (Fig. 1). All three methods attain an unprecedented level of comprehensiveness and sensitivity in off-target detection. The papers also highlight that the specificity of nucleases varies widely and must be evaluated case by case.
A powerful genome editing tool may soon become even more powerful. Researchers with the Lawrence Berkeley National Laboratory (Berkeley Lab) have unlocked the key to how bacteria are able to 'steal' genetic information from viruses and other foreign invaders for use in their own immunological memory ...
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